Leukemia: Acute promyelocytic leukemia https://greenmedinfo.com/taxonomy/term/17926/all en 20( S)-ginsenoside Rh2 induces caspase-dependent promyelocytic leukemia. https://greenmedinfo.com/article/20-s-ginsenoside-rh2-induces-caspase-dependent-promyelocytic-leukemia PMID:  J Ginseng Res. 2021 Mar ;45(2):295-304. Epub 2020 May 15. PMID: 33841010 Abstract Title:  20()-ginsenoside Rh2 induces caspase-dependent promyelocytic leukemia-retinoic acid receptor A degradation in NB4 cells via Akt/Bax/caspase9 and TNF-α/caspase8 signaling cascades. Abstract:  Background: Acute promyelocytic leukemia (APL) is a hematopoietic malignancy driven by promyelocytic leukemia-retinoic acid receptor A (PML-RARA) fusion gene. The therapeutic drugs currently used to treat APL have adverse effects. 20()-ginsenoside Rh2 (GRh2) is an anticancer medicine with high effectiveness and low toxicity. However, the underlying anticancer mechanisms of GRh2-induced PML-RARA degradation and apoptosis in human APL cell line (NB4 cells) remain unclear.Methods: Apoptosis-related indicators and PML-RARA expression were determined to investigate the effect of GRh2 on NB4 cells. Z-VAD-FMK, LY294002, and C 87, as inhibitors of caspase, and the phosphatidylinositol 3-kinase (PI3K) and tumor necrosis factor-α (TNF-α ) pathways were used to clarify the relationship between GRh2-induced apoptosis and PML-RARA degradation.Results: GRh2 dose- and time-dependently decreased NB4 cell viability. GRh2-induced apoptosis, cell cycle arrest, and caspase3, caspase8, and caspase9 activation in NB4 cells after a 12-hour treatment. GRh2-induced apoptosis in NB4 cells was accompanied by massive production of reactive oxygen species, mitochondrial damage and upregulated Bax/Bcl-2 expression. GRh2 also induced PML/PML-RARA degradation, PML nuclear bodies formation, and activation of the downstream p53 pathway in NB4 cells. Z-VAD-FMK inhibited caspase activation and significantly reversed GRh2-induced apoptosis and PML-RARA degradation. GRh2 also upregulated TNF-α expression and inhibited Akt phosphorylation. LY294002, an inhibitor of the PI3K pathway, enhanced the antitumor effects of GRh2, and C 87, an inhibitor of the TNF-α pathway, reversed NB4 cell viability, and GRh2-mediated apoptosis in a caspase-8-dependent manner.Conclusion: GRh2 induced caspase-dependent PML-RARA degradation and apoptosis in NB4 cells via the Akt/Bax/caspase9 and TNF-α/caspase8 pathways. <p><a href="https://greenmedinfo.com/article/20-s-ginsenoside-rh2-induces-caspase-dependent-promyelocytic-leukemia" target="_blank">read more</a></p> https://greenmedinfo.com/article/20-s-ginsenoside-rh2-induces-caspase-dependent-promyelocytic-leukemia#comments Ginsenosides Leukemia: Acute promyelocytic leukemia Apoptotic In Vitro Study Thu, 15 Apr 2021 22:22:37 +0000 greenmedinfo 238005 at https://greenmedinfo.com 280 nm UV LED irradiation inhibits proliferation and induces apoptosis and necrosis in cultured HL-60 human leukemia cells. https://greenmedinfo.com/article/280-nm-uv-led-irradiation-inhibits-proliferation-and-induces-apoptosis-and-nec PMID:  Mol Med Rep. 2016 Mar ;13(3):2506-10. Epub 2016 Jan 27. PMID: 26820261 Abstract Title:  Ultraviolet light-emitting diode irradiation-induced cell death in HL-60 human leukemia cells in vitro. Abstract:  Ultraviolet (UV) radiation is considered to be a potent cell-damaging agent in various cell lineages; however, the effect of UV light‑emitting diode (LED) irradiation on human cells remains unclear. The aim of the present study was to examine the effect of UV LED irradiation emitting at 280 nm on cultured HL‑60 human leukemia cells, and to explore the underlying mechanisms. HL‑60 cells were irradiated with UV LED (8, 15,30 and 60 J/m2) and incubated for 2 h after irradiation. The rates of cell proliferation and apoptosis, the cell cycle profiles and the mRNA expression of B‑cell lymphoma 2 (Bcl‑2) were detected using cell counting kit‑8, multicaspase assays, propidium iodide staining and reverse transcription‑quantitative polymerase chain reaction, respectively. The results showed that UV LED irradiation (8‑60 J/m2) inhibited the proliferation of HL‑60 cells in a dose‑dependent manner. UV LED at 8‑30 J/m2 induced dose‑dependent apoptosis and G0/G1 cell cycle arrest, and inhibited theexpression of Bcl‑2 mRNA, while UV LED at 60 J/m2 induced necrosis. In conclusion, 280 nm UV LED irradiation inhibits proliferation and induces apoptosis and necrosis in cultured HL‑60 cells. In addition, the cell cycle arrest at the G0/G1 phase and the downregulation of Bcl‑2 mRNA expression were shown to be involved in UV LED-induced apoptosis. https://greenmedinfo.com/article/280-nm-uv-led-irradiation-inhibits-proliferation-and-induces-apoptosis-and-nec#comments Leukemia: Acute promyelocytic leukemia Antiproliferative Apoptotic Bcl-2 protein down-regulation Cell cycle arrest Light-Emitting Diodes (LEDs) Therapy Dose Response In Vitro Study Wed, 13 Apr 2016 01:32:44 +0000 greenmedinfo 125906 at https://greenmedinfo.com Acteoside inhibits human promyelocytic HL-60 leukemia cell proliferation. https://greenmedinfo.com/article/acteoside-inhibits-human-promyelocytic-hl-60-leukemia-cell-proliferation PMID:  Carcinogenesis. 2007 Sep ;28(9):1928-36. Epub 2007 Jul 18. PMID: 17634406 Abstract Title:  Acteoside inhibits human promyelocytic HL-60 leukemia cell proliferation via inducing cell cycle arrest at G0/G1 phase and differentiation into monocyte. Abstract:  We investigated the in vitro effects of acteoside on the proliferation, cell cycle regulation and differentiation of HL-60 human promyelocytic leukemia cells. Acteoside inhibited the proliferation of HL-60 cells in a concentration- and time-dependent manner with an IC50, approximately 30 microM. DNA flow cytometric analysis indicated that acteoside blocked cell cycle progression at the G1 phase in HL-60 human promyelocytic leukemia cells. Among the G1 phase cell cycle-related proteins, the levels of cyclin-dependent protein kinase (CDK)2, CDK6, cyclin D1, cyclin D2, cyclin D3 and cyclin E were reduced by acteoside, whereas the steady-state level of CDK4 was unaffected. The protein and mRNA levels of CDK inhibitors (cyclin-dependent kinase inhibitors), such as p21(CIP1/WAF1) and p27(KIP1), were gradually increased after acteoside treatment in a time-dependent manner. In addition, acteoside markedly enhanced the binding of p21(CIP1/WAF1) and p27(KIP1) to CDK4 and CDK6, resulting in the reduction of CDK2, CDK4 and CDK6 activities. Moreover, the hypophosphorylated form of retinoblastoma increased, leading to the enhanced binding of protein retinoblastoma (pRb) and E2F1. Our results further suggest that acteoside is a potent inducer of differentiation of HL-60 cells based on biochemical activities and the expression level of CD14 cell surface antigen. In conclusion, the onset of acteoside-induced G1 arrest of HL-60 cells prior to the differentiation appears to be tightly linked to up-regulation of the p21(CIP1/WAF1) and p27(KIP1) levels and decreases in the CDK2, CDK4 and CDK6 activities. These findings, for the first time, reveal the mechanism underlying the anti-proliferative effect of acteoside on human promyelocytic HL-60 cells. <p><a href="https://greenmedinfo.com/article/acteoside-inhibits-human-promyelocytic-hl-60-leukemia-cell-proliferation" target="_blank">read more</a></p> https://greenmedinfo.com/article/acteoside-inhibits-human-promyelocytic-hl-60-leukemia-cell-proliferation#comments Leukemia: Acute promyelocytic leukemia Verbascoside Antiproliferative Cell cycle arrest P21 Activation In Vitro Study Wed, 12 Sep 2018 19:21:36 +0000 greenmedinfo 170520 at https://greenmedinfo.com Ameliorative effects and mechanism of crocetin in arsenic trioxide‑induced cardiotoxicity. https://greenmedinfo.com/article/ameliorative-effects-and-mechanism-crocetin-arsenic-trioxide-induced-cardiotox PMID:  Mol Med Rep. 2020 Dec ;22(6):5271-5281. Epub 2020 Oct 14. PMID: 33173984 Abstract Title:  Ameliorative effects and mechanism of crocetin in arsenic trioxide‑induced cardiotoxicity in rats. Abstract:  Arsenic trioxide (ATO) is commonly used to treat patients with acute promyelocytic leukemia since it was authorized by the U.S. Food and Drug Administration in the 1970s, but its applicability has been limited by its cardiotoxic effects. Therefore, the aim of the present study was to investigate the cardioprotective effects and underlying mechanism of crocetin (CRT), the critical ingredient of saffron. Sprague‑Dawley rats were then randomly divided into four groups (n=10/group): i) Control group; ii) ATO group, iii) CRT‑low (20 mg/kg) group; and iv) CRT‑high (40 mg/kg) group. Rats in the Control and ATO groups were intraperitoneally injected with equal volumes of 0.9% sodium chloride solution, and CRT groups were administered with either 20 and 40 mg/kg CRT. Following 6 h, all groups except the Control group were intraperitoneally injected with 5 mg/kg ATO over 10 days. Cardiotoxicity was indicated by changes in electrocardiographic (ECG) patterns, morphology and marker enzymes. Histomorphological changes in the heart tissue were observed by pathological staining. The levels of superoxide dismutase, glutathione peroxidase, malondialdehyde and catalase in the serum were analyzed using colometric commercial assay kits, and the levels of reactive oxygen species in the heart tissue were detected using the fluorescent probe dihydroethidium. The expression levels of inflammatory factors and activities of apoptosis‑related proteins were analyzed using immunohistochemistry. The protein expression levels of silent information regulator of transcription 1 were measured using western blotting. Cardiotoxicity was induced in male Sprague‑Dawley rats with ATO (5 mg/kg). CRT (20 and 40 mg/kg) and ATO were co‑administered to evaluate possible cardioprotective effects. CRT significantly reduced the heart rate and J‑point elevation induced by ATO in rats. Histologicalchanges were evaluated via hematoxylin and eosin staining. CRT decreased the levels of creatine kinase and lactate dehydrogenase, increased the activities of superoxide dismutase, glutathione‑peroxidase and catalase, and decreased the levels of malondialdehyde and reactive oxygen species. Moreover, CRT downregulated the expression levels of the pro‑inflammatory factors IL‑1, TNF‑α, IL‑6, Bax and p65, as well as increased the expression of Bcl‑2. It was also identified that CRT enhanced silent information regulator of transcription 1 protein expression. Thus, the present study demonstrated that CRT treatment effectively ameliorated ATO‑induced cardiotoxicity. The protective effects of CRT can be attributed to the inhibition of oxidative stress, inflammation and apoptosis. Therefore, CRT represents a promising therapeutic method for improving the cardiotoxic side effects caused by ATO treatment, and additional clinical applications are possible, but warrant further investigation. <p><a href="https://greenmedinfo.com/article/ameliorative-effects-and-mechanism-crocetin-arsenic-trioxide-induced-cardiotox" target="_blank">read more</a></p> https://greenmedinfo.com/article/ameliorative-effects-and-mechanism-crocetin-arsenic-trioxide-induced-cardiotox#comments Arsenic Poisoning Chemotherapy-Induced Toxicity: Arsenic Trioxide Crocetin Leukemia: Acute promyelocytic leukemia Arsenic Trioxide Cardioprotective Animal Study Tue, 22 Dec 2020 21:08:17 +0000 greenmedinfo 231657 at https://greenmedinfo.com Anti-leukemia activity of polysaccharide from Sargassum fusiforme. https://greenmedinfo.com/article/anti-leukemia-activity-polysaccharide-sargassum-fusiforme PMID:  Mar Drugs. 2023 May 8 ;21(5). Epub 2023 May 8. PMID: 37233483 Abstract Title:  Anti-Leukemia Activity of Polysaccharide fromvia the PI3K/AKT/BAD Pathway In Vivo and In Vitro. Abstract:  Studies have shown thatand its extracts are effective herbal treatments for leukemia. We previously found that a polysaccharide from, SFP 2205, stimulated apoptosis in human erythroleukemia (HEL) cells. However, the structural characterization and antitumoral mechanisms of SFP 2205 remain uncertain. Here, we studied the structural characteristics and anticancer mechanisms of SFP 2205 in HEL cells and a xenograft mouse model. The results demonstrated that SFP 2205, with a molecular weight of 41.85 kDa, consists of mannose, rhamnose, galactose, xylose, glucose, and fucose with monosaccharides composition of 14.2%, 9.4%, 11.8%, 13.7%, 11.0%, and 38.3%, respectively. On animal assays, SFP 2205 significantly inhibited growth of HEL tumor xenografts with no discernible toxicity to normal tissues. Western blotting showed that SFP 2205 therapy improved Bad, Caspase-9, and Caspase-3 protein expression, and ultimately induced HEL tumor apoptosis, indicating mitochondrial pathway involvement. Furthermore, SFP 2205 blocked the PI3K/AKT signaling pathway and 740 Y-P, an activator of the PI3K/AKT pathway, rescued the effects of SFP 2205 on HEL cell proliferation and apoptosis. Overall, SFP 2205 may be a potential functional food additive or adjuvant for preventing or treating leukemia. <p><a href="https://greenmedinfo.com/article/anti-leukemia-activity-polysaccharide-sargassum-fusiforme" target="_blank">read more</a></p> https://greenmedinfo.com/article/anti-leukemia-activity-polysaccharide-sargassum-fusiforme#comments Leukemia: Acute promyelocytic leukemia Seaweed: Brown Apoptotic Polysaccharides Animal Study In Vitro Study Sun, 05 Nov 2023 20:53:48 +0000 greenmedinfo 282923 at https://greenmedinfo.com Anti-proliferative profile of Anacardium occidentale polysaccharide. https://greenmedinfo.com/article/anti-proliferative-profile-anacardium-occidentale-polysaccharide PMID:  Int J Biol Macromol. 2020 Aug 1 ;156:981-987. Epub 2020 Mar 16. PMID: 32194125 Abstract Title:  Anti-proliferative profile of Anacardium occidentale polysaccharide and characterization by AFM. Abstract:  This paper explores the application of cashew gum (CG) as an in vitro antiproliferative, firstly by isolating and characterizing the gum using elemental analysis, gel-permeation chromatography, nuclear magnetic resonance (NMR) and atomic force microscopy (AFM). The molar mass of isolated CG was in the order of 10-10 g/mol, with small protein traces present. Polymer characterization by NMR identified key signals correlating to galactose, glucose, rhamnose and acid-related groups. Three distinct conformational stages were observed by AFM. The impact of CG on cell morphology and viability with both tumor and non-tumor cell lines was studied by AFM and 3-(4,5-dimethyl-2-thiazole)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay respectively. Antiproliferative activity was confirmed for HCT116 (colorectal carcinoma), B16F10 (melanoma) and HL60 (promyelocytic leukemia) cancer cell lines. A change in cell morphology was demonstrated as an increased surface roughness for HL60. Considering that a CG does not exhibit cytotoxicity to non-tumor lines, it can be seen that the CG shows selectivity for tumor cells and can be a promising biomaterial for future studies. <p><a href="https://greenmedinfo.com/article/anti-proliferative-profile-anacardium-occidentale-polysaccharide" target="_blank">read more</a></p> https://greenmedinfo.com/article/anti-proliferative-profile-anacardium-occidentale-polysaccharide#comments Cashew Colorectal Cancer Leukemia: Acute promyelocytic leukemia Melanoma Antiproliferative Polysaccharides Selective Antiproliferation In Vitro Study Fri, 12 Jun 2020 20:36:04 +0000 greenmedinfo 221905 at https://greenmedinfo.com Anticancer and anti-inflammatory activities of shallot extract. https://greenmedinfo.com/article/anticancer-and-anti-inflammatory-activities-shallot-extract PMID:  Arch Med Sci. 2011 Feb ;7(1):38-44. Epub 2011 Mar 8. PMID: 22291731 Abstract Title:  Anticancer and anti-inflammatory activities of shallot (Allium ascalonicum) extract. Abstract:  INTRODUCTION: Alliumplants are an important part of the diet of many populations and there is a long-held belief in their health-enhancing properties such as cancer prevention. In this study, the anticancer and anti-inflammatory activities of the aqueous extract of the Allium ascalonicum bulbs have been studied.MATERIAL AND METHODS: The antiproliferative and anti-growth activity of the aqueous extract of A. ascalonicum was examined in vitro on different tumor cell lines. Furthermore, the acetic acid-induced vascular permeability as an in vivo assay was used for studying anti-inflammatory activity of the extract.RESULTS: The aqueous extract of A. ascalonicum had the most anti-growth activity on the cancer cell lines; Jurkat and K562 against Wehi 164 with lower cytotoxic preference. The extract also showed much less cytotoxicity against the normal cell (HUVEC) line and significant anti-inflammatory activity in vivo.CONCLUSIONS: It is of interest that the extract of this plant has shown much less cytotoxicity against the normal cell line, and, if this also occurs in vivo, the use of this plant clinically for the treatment of cancer patients would have some scientific support. The results of these assays indicated that A. ascalonicum can be a candidate for prevention and treatment of many diseases related to inflammation and malignancy. <p><a href="https://greenmedinfo.com/article/anticancer-and-anti-inflammatory-activities-shallot-extract" target="_blank">read more</a></p> https://greenmedinfo.com/article/anticancer-and-anti-inflammatory-activities-shallot-extract#comments Breast Cancer Cervical Cancer Inflammation Leukemia: Acute promyelocytic leukemia Shallot Anti-Inflammatory Agents Antiproliferative Plant Extracts In Vitro Study Wed, 15 Nov 2017 23:23:16 +0000 greenmedinfo 155859 at https://greenmedinfo.com Antileukemic, antioxidant, anti-inflammatory and healing activities induced by a polyphenol-enriched fraction extracted from leaves of myrtus. https://greenmedinfo.com/article/antileukemic-antioxidant-anti-inflammatory-and-healing-activities-induced-poly PMID:  Nutrients. 2022 Nov 27 ;14(23). Epub 2022 Nov 27. PMID: 36501085 Abstract Title:  Antileukemic, Antioxidant, Anti-Inflammatory and Healing Activities Induced by a Polyphenol-Enriched Fraction Extracted from Leaves ofL. Abstract:  Natural products have offered a number of exciting approaches in cancer treatment over the years. In this study, we investigated the prophylactic and therapeutic effects of the polyphenol-enriched fraction extracted from(PEMC) on acute and chronic leukemia. According to the UHPLC-MS, the fraction is rich in flavonoids. Protective activity of the PEMC was assessed by evaluating the antioxidant, anti-inflammatory, wound healing, and hemolysis potential in a series of in vivo and in vitro assays, while the therapeutic approach consisted of the evaluation of cytotoxic activity of the PEMC against HL60 and K562 leukemia cell lines. Safety of the fraction was also evaluated on a non-cancerous Vero cell line and by an acute toxicity test performed in mice. The PEMC demonstrated a significant anti-inflammatory and healing potential. The activities found at the dose of 100 mg/kg were better than those observed using a reference drug. The PEMC demonstrated a significant antioxidant effect and a specific cytotoxicity towards HL60 (IC= 19.87µM) and K562 (IC= 29.64µM) cell lines being non-toxic to the Vero cell line. No hemolytic activity was observed in vitro and no toxicity effect was found in mice. Thus, the PEMC has a pharmacological potential as both preventive and therapeutic agent. However, further research is necessary to propose its mechanism of action. <p><a href="https://greenmedinfo.com/article/antileukemic-antioxidant-anti-inflammatory-and-healing-activities-induced-poly" target="_blank">read more</a></p> https://greenmedinfo.com/article/antileukemic-antioxidant-anti-inflammatory-and-healing-activities-induced-poly#comments Leukemia: Acute promyelocytic leukemia Myrtle Polyphenols Anti-Inflammatory Agents Antioxidants Chemopreventive Plant Extracts Animal Study Mon, 12 Jun 2023 22:31:42 +0000 greenmedinfo 274678 at https://greenmedinfo.com Apoptosis of NB4 cells was induced by puerarin in vitro. https://greenmedinfo.com/article/apoptosis-nb4-cells-was-induced-puerarin-vitro PMID:  Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2010 Apr ;18(2):326-9. PMID: 20416161 Abstract Title:  [Apoptosis of NB4 cells induced by flavonoids of puerarin in vitro]. Abstract:  This study was aimed to investigate the effects of flavonoids of puerarin (PR) on apoptosis of acute promyelocytic leukemia (APL) cell line NB4 cells and its mechanism. The NB4 were treated with PR in vitro, the MTT assay was used to detect the inhibitory effect of PR on cell proliferation. The apoptosis of NB4 cells were detected by flow cytometry labelled with Annexin V/PI. The expressions of pml/rar alpha, bcl-2 and survivin were detected by real time reverse transcription-polymerase chain reaction (real time RT-PCR), the expressions of JNK, p38 MAPK, FasL, caspase 3, caspase 8 were detected by Western blot. The results showed that with the increasing of PR concentrations, the apoptosis rates of NB4 cells were gradually elevated. Simultaneously, the mRNA expression of pml/rar alpha, bcl-2 and survivin decreased, while the protein expression of JNK, FasL, caspase 3 and caspase 8 increased, which presented the positive correlation to PR concentrations. When PR combined with arsenic trioxide (ATO), the expression levels of above mentioned mRNA and protein decreased or increased more significantly. It is concluded that PR can effectively induce the apoptosis of NB4 cells. PR combined with ATO displays synergistic effect. It may be triggered by the activation of JNK signal pathway. <p><a href="https://greenmedinfo.com/article/apoptosis-nb4-cells-was-induced-puerarin-vitro" target="_blank">read more</a></p> https://greenmedinfo.com/article/apoptosis-nb4-cells-was-induced-puerarin-vitro#comments Leukemia: Acute promyelocytic leukemia Puerarin Antiproliferative Apoptotic In Vitro Study Thu, 07 Jun 2018 00:49:35 +0000 greenmedinfo 165406 at https://greenmedinfo.com Apoptosis-inducing effect of quercetin and kaempferol on human HL-60 cells and its mechanism. https://greenmedinfo.com/article/apoptosis-inducing-effect-quercetin-and-kaempferol-human-hl-60-cells-and-its-m PMID:  Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2010 Jun ;18(3):629-33. PMID: 20561416 Abstract Title:  [Apoptosis-inducing effect of quercetin and kaempferol on human HL-60 cells and its mechanism]. Abstract:  The purpose of this study was to explore the anti-leukemia effect of quercetin and kaempferol and its mechanism. The HL-60 cells were used as the leukemia models. The inhibitory effects of quercetin and kaempferol on growth of HL-60 cells was assessed by MTT assay. The effect of quercetin and kaempferol on cell cycle in HL-60 cells was detected by flow cytometry. The cytotoxic effect of these 2 drugs was analysed by single cell electrophoresis assay. Western blot analysis was used to study the apoptotic mechanism of HL-60 cells. The results showed that the quercetin and kaempferol had a significant anti-leukemia effect in vitro. The proliferation of HL-60 cells was significantly inhibited in dose-and time-dependent manners after treating with quercetin (r = 0.77) and kaempferol (r = 0.76) respectively, and the cytotoxicity of quercetin was superior to that of kaempferol. The quercetin and kaempferol induced G(2)/M arrest and apoptosis of HL-60 cells. The quercetin and kaempferol could down-regulate the survivin expression. It is concluded that the quercetin and kaempferol have significant anti-leukemia effect in vitro. Furthermore the apoptosis-inducing effect of quercetin is stronger than that of kaempferol, both of which induce apoptosis of HL-60 cells through depressing cell growth, arresting cell cycle and inhibiting expression of survivin. <p><a href="https://greenmedinfo.com/article/apoptosis-inducing-effect-quercetin-and-kaempferol-human-hl-60-cells-and-its-m" target="_blank">read more</a></p> https://greenmedinfo.com/article/apoptosis-inducing-effect-quercetin-and-kaempferol-human-hl-60-cells-and-its-m#comments Kaempferol Leukemia: Acute promyelocytic leukemia Quercetin Antiproliferative Apoptotic Cell cycle arrest In Vitro Study Sun, 24 Nov 2019 03:25:01 +0000 greenmedinfo 202706 at https://greenmedinfo.com Astragalus membranaceus saponins can be used in the treatment of inflammatory diseases and inflammation-mediated tumor development. https://greenmedinfo.com/article/astragalus-membranaceus-saponins-can-be-used-treatment-inflammatory-diseases-a PMID:  Am J Chin Med. 2016 Apr 24:1-15. Epub 2016 Apr 24. PMID: 27109155 Abstract Title:  Astragalus saponins Inhibits Lipopolysaccharide-Induced Inflammation in Mouse Macrophages. Abstract:  Excessive nitric oxide (NO) and pro-inflammatory cytokines are produced during the pathogenesis of inflammatory diseases and cancer. It has been demonstrated that anti-inflammation contributes Astragalus membranaceus saponins (AST)&#039;s beneficial effects in combination of conventional anticancer drugs. However, the immunomodulating property of AST has not been well characterized. In this study, we found that AST suppressed lipopolysaccharide (LPS)-induced generation of NO without causing cytotoxicity in the mouse macrophage RAW264.7. The gene and protein overexpression of inducible NO synthase (iNOS) as well as the production of tumor necrosis factor-[Formula: see text], evoked by LPS, was consistently down-regulated by AST. AST also inhibited the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and suppressed nuclear factor (NF)-[Formula: see text]B activation and the associated I[Formula: see text]B[Formula: see text] degradation during LPS insult. Furthermore, AST induced growth inhibition in promyelocytic leukemic HL-60 cells and T-lymphocyte leukemic Jurkat cells, but exerted no cytotoxic effects in normal human peripheral blood mononuclear cells (PBMC). It is known that the chemotherapeutic drug 5-FU can suppress the immune system, which can be identified by a reduced white blood cell count and decreased hematocrit, while the combination of AST and 5-FU can reverse the above hematologic toxicities. To summarize, non-cytotoxic concentrations of AST suppress LPS-induced inflammatory responses via the modulation of p38 MAPK signaling and the inhibition of NO and cytokine release. Importantly, AST can alleviate the hematologic side effects of current chemotherapeutic agents. These findings can facilitate the establishment of AST in the treatment of inflammatory diseases and inflammation-mediated tumor development. https://greenmedinfo.com/article/astragalus-membranaceus-saponins-can-be-used-treatment-inflammatory-diseases-a#comments Astragalus Leukemia Leukemia: Acute promyelocytic leukemia Lipopolysaccharide-Induced Toxicity Antioxidants Chemoprotective Agents Immunomodulatory In Vitro Study Wed, 27 Apr 2016 01:02:36 +0000 greenmedinfo 126540 at https://greenmedinfo.com Berberine induces apoptotic cell death in HL-60 human leukemia cells. https://greenmedinfo.com/article/berberine-induces-apoptotic-cell-death-hl-60-human-leukemia-cells PMID:  Am J Chin Med. 2017 ;45(7):1497-1511. PMID: 29025293 Abstract Title:  Berberine Induces Apoptotic Cell Death via Activation of Caspase-3 and -8 in HL-60 Human Leukemia Cells: Nuclear Localization and Structure-Activity Relationships. Abstract:  Berberine (BBR), an isoquinoline alkaloid, is a well-known bioactive compound contained in medicinal plants used in traditional and folk medicines. In this study, we investigated the subcellular localization and the apoptotic mechanisms of BBR were elucidated. First, we confirmed the incorporation of BBR into the cell visually. BBR showed antiproliferative activity and promptly localized to the nucleus from 5[Formula: see text]min to 15[Formula: see text]min after BBR treatment in HL-60 human promyelocytic leukemia cells. Next, we examined the antiproliferative activity of BBR (1) and its biosynthetically related compounds (2-7) in HL-60 cells. BBR exerted strongest antiproliferative activity among 1-7 and the results of structures and activity relation suggested that a methylenedioxyl group in ring A, an [Formula: see text]-alkyl group at C-9 position, and the frame of isoquinoline may be necessary for antiproliferative activity. Moreover, BBR showed the most potent antiproliferative activity in HL-60 cells among human cancer and normal cell lines tested. Next, we examined the effect of BBR on molecular events known as apoptosis induction. In HL-60 cells, BBR induced chromatin condensation and DNA fragmentation, and triggered the activation of PARP, caspase-3 and caspase-8 without the activation of caspase-9. BBR-induced DNA fragmentation was abolished by pretreatment with inhibitors against caspase-3 and caspase-8, but not against caspase-9. ERK and p38 were promptly phosphorylated after 15 min of BBR treatment, and this was correlated with time of localization to the nucleus of BBR. These results demonstrated that BBR translocated into nucleus immediately after treatments and induced apoptotic cell death by activation of caspase-3 and caspase-8. <p><a href="https://greenmedinfo.com/article/berberine-induces-apoptotic-cell-death-hl-60-human-leukemia-cells" target="_blank">read more</a></p> https://greenmedinfo.com/article/berberine-induces-apoptotic-cell-death-hl-60-human-leukemia-cells#comments Berberine Leukemia: Acute promyelocytic leukemia Antiproliferative Apoptotic In Vitro Study Fri, 27 Oct 2017 03:49:50 +0000 greenmedinfo 154948 at https://greenmedinfo.com Cinnamon extract inhibit the tumor cell survival by both down-regulated their target cell cycle regulation molecules and mitosis regulation molecules. https://greenmedinfo.com/article/cinnamon-extract-inhibit-tumor-cell-survival-both-down-regulated-their-target- PMID:  Eur Rev Med Pharmacol Sci. 2018 08 ;22(16):5347-5354. PMID: 30178861 Abstract Title:  Proliferation effects of cinnamon extract on human HeLa and HL-60 tumor cell lines. Abstract:  OBJECTIVE: To investigate the possible anti-cancer properties of cinnamon extract on two human tumor cell lines, HeLa cells and HL-60 cells.MATERIALS AND METHODS: Two human tumor cell lines, HeLa cells and HL-60 cells, were exposed to increased concentrations of an extract prepared from cinnamon. The cell proliferation and cell cycle distribution were evaluated using MTT assay and flow cytometry, respectively. The possible action mechanism was also investigated by Western blot.RESULTS: The results showed that cinnamon extract strongly inhibited tumor cell proliferation in a dose-dependent manner and exhibited dramatic increases in the percentage of cells in G2/M in parallel with exposure to increasing concentration of cinnamon extract. The Western blot results showed that cinnamon extract reduced the cyclin A, cyclin B1, ERK2, and p-ERK proteins expression.CONCLUSIONS: Our study suggested that cinnamon extract inhibit the tumor cell survival by both down-regulated their target cell cycle regulation molecules and mitosis regulation molecules. <p><a href="https://greenmedinfo.com/article/cinnamon-extract-inhibit-tumor-cell-survival-both-down-regulated-their-target-" target="_blank">read more</a></p> https://greenmedinfo.com/article/cinnamon-extract-inhibit-tumor-cell-survival-both-down-regulated-their-target-#comments Cervical Cancer Cinnamon Leukemia: Acute promyelocytic leukemia Antiproliferative Apoptotic Cell cycle arrest Plant Extracts In Vitro Study Sun, 17 Nov 2019 22:33:05 +0000 greenmedinfo 202054 at https://greenmedinfo.com Cucurbitacin B synergistically enhances the apoptosis-inducing effect of arsenic trioxide by inhibiting STAT3 phosphorylation in Ramos cells. https://greenmedinfo.com/article/cucurbitacin-b-synergistically-enhances-apoptosis-inducing-effect-arsenic-trio PMID:  Leuk Lymphoma. 2017 Feb 20:1-13. Epub 2017 Feb 20. PMID: 28278714 Abstract Title:  Cucurbitacin B synergistically enhances the apoptosis-inducing effect of arsenic trioxide by inhibiting STAT3 phosphorylation in lymphoma Ramos cells. Abstract:  Arsenic trioxide (ATO) is a classic apoptosis-inducing agent used to treat acute promyelocytic leukemia. However, the therapeutic effect of ATO is limited in lymphoma, which resists apoptosis possibly due to inappropriate activation of STAT3. Therefore, combination of ATO and STAT3 inhibitor may be a potential strategy to treat lymphoma. Dramatically, Cucurbitacin B (CuB), an effective component of the dichloromethane extraction from Trichosanthes kirilowii Maxim, synergistically eliminated the apoptosis resistance of Burkitt&#039;s lymphoma Ramos cells to ATO by inhibiting the phosphorylation of STAT3, followed in turn by downregulation of Bcl-2 and upregulation of Bax. Furthermore, CuB and ATO in combination have no pro-apoptotic effect on normal lymphatic cells, indicating the absence of toxicity to hematological cells. This synergistic effect was further confirmed in nude murine lymphoma model, which exhibited significant apoptosis induction and tumor growth inhibition. Collectively, CuB synergistically enhances the apoptosis-inducing effect of ATO by inhibiting STAT3 phosphorylation in Ramos cells. <p><a href="https://greenmedinfo.com/article/cucurbitacin-b-synergistically-enhances-apoptosis-inducing-effect-arsenic-trio" target="_blank">read more</a></p> https://greenmedinfo.com/article/cucurbitacin-b-synergistically-enhances-apoptosis-inducing-effect-arsenic-trio#comments Cucurbitacin B Leukemia: Acute promyelocytic leukemia Apoptotic Arsenic Trioxide Chemosensitizer Chemotherapeutic In Vitro Study Tue, 06 Jun 2017 23:06:26 +0000 greenmedinfo 148759 at https://greenmedinfo.com Curcumin induces programmed cell death in human promyelocytic leukemia HL-60 cells. https://greenmedinfo.com/article/curcumin-induces-programmed-cell-death-human-promyelocytic-leukemia-hl-60-cell PMID:  Life Sci. 2008 Feb 13;82(7-8):367-75. Epub 2007 Dec 7. PMID: 18187158 Abstract Title:  Curcumin induces apoptosis through an ornithine decarboxylase-dependent pathway in human promyelocytic leukemia HL-60 cells. Abstract:  Curcumin, a well-known dietary pigment derived from the food flavoring turmeric (Curcuma longa) exhibits anti-proliferative, anti-inflammatory, and anti-oxidative activities. Recently, studies have shown that a chemopreventive effect of curcumin could be due to the hyperproduction of reactive oxygen species (ROS) inducing apoptosis in tumor cells. In our previous studies, ornithine decarboxylase (ODC) overexpression prevented tumor necrosis factor alpha (TNF-alpha)- and methotrexate-induced apoptosis via reduction of ROS. Furthermore, ODC is the rate-limiting enzyme in polyamine biosynthesis and a target for chemoprevention. In this study, we found that enzyme activity and protein expression of ODC were reduced during curcumin treatment. Overexpression of ODC in human promyelocytic leukemia HL-60 parental cells could reduce curcumin-induced apoptosis, which leads to loss of mitochondrial membrane potential (Deltapsi(m)), through reducing intracellular ROS. Moreover, ODC overexpression prevented cytochrome c release and the activation of caspase-9 and caspase-3 following curcumin treatment. These results demonstrate that curcumin-induced apoptosis occurs through a mechanism of down-regulating ODC and along a ROS-dependent mitochondria-mediated pathway. https://greenmedinfo.com/article/curcumin-induces-programmed-cell-death-human-promyelocytic-leukemia-hl-60-cell#comments Curcumin Leukemia: Acute promyelocytic leukemia Anticarcinogenic Agents Antioxidants Apoptotic In Vitro Study Sat, 12 Feb 2011 04:30:16 +0000 greenmedinfo 61490 at https://greenmedinfo.com