Cachexia: Chemotherapy Induced https://greenmedinfo.com/taxonomy/term/75038/all en 5-FU was found to induce a reduction in food intake in mice. https://greenmedinfo.com/article/5-fu-was-found-induce-reduction-food-intake-mice PMID:  Clin Exp Pharmacol Physiol. 2016 Apr 30. Epub 2016 Apr 30. PMID: 27130783 Abstract Title:  Role of peptide YY in 5-fluorouracil-induced reduction of dietary intake. Abstract:  5-fluorouracil (5-FU) is part of the standard care for cancer treatment but is associated with high incidences of appetite loss and reduced food intake, which may contribute to chemotherapy-induced cachexia (weakness and wasting of tissue). The role of gastrointestinal satiety hormones in chemotherapy-induced appetite loss has not been intensively investigated. Peptide YY (PYY) and glucagon-like peptide (GLP)-1 are important signals of gastrointestinal satiety, so we examined the roles of these gut hormones in 5-FU-induced reduction of dietary intake. Mice were given 5-FU (50 mg/kg, i.p.) every day for 4 consecutive days. Gene expression levels of proglucagon (Pro-Gcg), a precursor of GLP-1, and PYY in the colon were examined by real-time RT-PCR. Serum levels of GLP-1 and PYY were measured by enzyme-linked immunosorbent assay. Some mice were pretreated with the GLP-1 receptor antagonist exendin9-39 (1 mg/kg) or the neuropeptide Y type 2 (NPY2) receptor antagonist BIIE0246 (2 mg/kg) via the intraperitoneal route 30 min before 5-FU administration. Mice receiving 5-FU exhibited a significant reduction in food intake that was correlated with body weight loss. These mice also showed significantly enhanced expression levels of mRNAs encoding pro-GLP-1 and PYY in the transverse and distal colon as well as elevated serum concentrations of GLP-1 and PYY compared to vehicle-treated controls. The 5-FU-induced reduction in food intake was attenuated by BIIE0246 but not by exendin9-39. These data suggest that administration of a NPY2 receptor antagonist may be effective for attenuating the anorexia caused by 5-FU chemotherapy. This article is protected by copyright. All rights reserved. https://greenmedinfo.com/article/5-fu-was-found-induce-reduction-food-intake-mice#comments Anorexia: Cancer-Associated Cachexia: Chemotherapy Induced Chemotherapy-Induced Toxicity: 5-fluorouracil Fluorouracil (5-FU or f5U) Animal Study Mon, 02 May 2016 14:24:05 +0000 greenmedinfo 126766 at https://greenmedinfo.com Cannabigerol is able to stimulate appetite in pre-satiated rats. https://greenmedinfo.com/article/cannabigerol-able-stimulate-appetite-pre-satiated-rats PMID:  Psychopharmacology (Berl). 2016 Aug 9. Epub 2016 Aug 9. PMID: 27503475 Abstract Title:  Cannabigerol is a novel, well-tolerated appetite stimulant in pre-satiated rats. Abstract:  RATIONALE: The appetite-stimulating properties of cannabis are well documented and have been predominantly attributed to the hyperphagic activity of the psychoactive phytocannabinoid,∆(9)-tetrahydrocannabinol (∆(9)-THC). However, we have previously shown that a cannabis extract devoid of ∆(9)-THC still stimulates appetite, indicating that other phytocannabinoids also elicit hyperphagia. One possible candidate is the non-psychoactive phytocannabinoid cannabigerol (CBG), which has affinity for several molecular targets with known involvement in the regulation of feeding behaviour. OBJECTIVES: The objective of the study was to assess the effects of CBG on food intake and feeding pattern microstructure. METHODS: Male Lister hooded rats were administered CBG (30-120 mg/kg, per ora (p.o.)) or placebo and assessed in open field, static beam and grip strength tests to determine a neuromotor tolerability profile for this cannabinoid. Subsequently, CBG (at 30-240 mg/kg, p.o.) or placebo was administered to a further group of pre-satiated rats, and hourly intake and meal pattern data were recorded over 2 h. RESULTS: CBG produced no adverse effects on any parameter in the neuromotor tolerability test battery. In the feeding assay, 120-240 mg/kg CBG more than doubled total food intake and increased the number of meals consumed, and at 240 mg/kg reduced latency to feed. However, the sizes or durations of individual meals were not significantly increased. CONCLUSIONS: Here, we demonstrate for the first time that CBG elicits hyperphagia, by reducing latency to feed and increasing meal frequency, without producing negative neuromotor side effects. Investigation of the therapeutic potential of CBG for conditions such as cachexia and other disorders of eating and body weight regulation is thus warranted. https://greenmedinfo.com/article/cannabigerol-able-stimulate-appetite-pre-satiated-rats#comments Cachexia Cachexia: Chemotherapy Induced Cannabigerol Cannabinoids Appetite Stimulants Animal Study Tue, 06 Sep 2016 21:12:52 +0000 greenmedinfo 134676 at https://greenmedinfo.com Capsaicin alleviates cisplatin-induced muscle loss and atrophy in vitro and in vivo. https://greenmedinfo.com/article/capsaicin-alleviates-cisplatin-induced-muscle-loss-and-atrophy-vitro-and-vivo PMID:  J Cachexia Sarcopenia Muscle. 2022 Nov 18. Epub 2022 Nov 18. PMID: 36401337 Abstract Title:  Capsaicin alleviates cisplatin-induced muscle loss and atrophy in vitro and in vivo. Abstract:  BACKGROUND: Cisplatin (CP) is a widely used chemotherapeutic drug with subsequent adverse effects on different organs and tissues including skeletal muscle loss and atrophy as the most common clinical symptoms. The molecular mechanism of cisplatin-induced muscle atrophy is not clearly understood. However, recent significant advances indicate that it is related to an imbalance in both the protein status and apoptosis. Capsaicin (CAP) is one of the major ingredients in chilli peppers. It is a valuable pharmacological agent with several therapeutic applications in controlling pain and inflammation with particular therapeutic potential in muscle atrophy. However, the mechanisms underlying its protective effects against cisplatin-induced muscle loss and atrophy remain largely unknown. This study aims to investigate capsaicin&#039;s beneficial effects on cisplatin-induced muscle loss and atrophy in vitro and in vivo.METHODS: The anti-muscle-atrophic effect of capsaicin on cisplatin-induced muscle loss was investigated using in vivo and in vitro studies. By using the pretreatment model, pretreated capsaicin for 24 h and treated with cisplatin for 48 h, we utilized a CCmyotube formation model where cell viability analysis, immunofluorescence, and protein expression were measured to investigate the effect of capsaicin in hampering cisplatin-induced muscle atrophy. C57BL/6 mice were administered capsaicin (10, 40 mg/kg BW) as a pretreatment for 5 weeks and cisplatin (3 mg/kg BW) for seven consecutively days to assess muscle atrophy in an animal model for protein and oxidative stress examination, and the grip strength was tested to evaluate the muscle strength.RESULTS: Our study results indicated that cisplatin caused lower cell viability and showed a subset of hallmark signs typically recognized during atrophy, including severe reduction in the myotube diameter, repression of Akt, and mTOR protein expression. However, pretreatment with capsaicin could ameliorate cisplatin-induced muscle atrophy by up-regulating the protein synthesis in skeletal muscle as well as down-regulating the markers of protein degradation. Additionally, capsaicin was able to downregulate the protein expression of apoptosis-related markers, activated TRPV1 and autophagy progress modulation and the recovery of lysosome function. In vivo, capsaicin could relieve oxidative stress and cytokine secretion while modulating autophagy-related lysosome fusion, improving grip strength, and alleviating cisplatin-induced body weight loss and gastrocnemius atrophy.CONCLUSIONS: These findings suggest that capsaicin can restore cisplatin-induced imbalance between protein synthesis and protein degradation pathways and it may have protective effects against cisplatin-induced muscle atrophy. <p><a href="https://greenmedinfo.com/article/capsaicin-alleviates-cisplatin-induced-muscle-loss-and-atrophy-vitro-and-vivo" target="_blank">read more</a></p> https://greenmedinfo.com/article/capsaicin-alleviates-cisplatin-induced-muscle-loss-and-atrophy-vitro-and-vivo#comments Cachexia: Chemotherapy Induced Capsaicin Chemotherapy-Induced Toxicity: Cisplatin Anti-Cachexic Agents Chemoprotective Agents Animal Study In Vitro Study Wed, 07 Dec 2022 01:31:07 +0000 greenmedinfo 267523 at https://greenmedinfo.com Chemotherapy inhibited tumor growth but promoted cachexia, this was attenuated by a combination of fish oil and selenium in this animal study. https://greenmedinfo.com/article/chemotherapy-inhibited-tumor-growth-promoted-cachexia-was-attenuated-combinati PMID:  Oncotarget. 2015 Apr 10 ;6(10):7758-73. PMID: 25797259 Abstract Title:  Skeletal muscle atrophy is attenuated in tumor-bearing mice under chemotherapy by treatment with fish oil and selenium. Abstract:  Chemotherapy can cause cachexia, which is manifested by weight loss, inflammation and muscle atrophy. However, the mechanisms of tumor and chemotherapy on skeletal muscle proteolysis, remained unclear. In this report, we demonstrated that tumor-induced myostatin in turn induced TNF-α, thus activating calcium-dependent and proteasomal protein degradation. Chemotherapy activated myostatin-mediated proteolysis and muscle atrophy by elevating IL-6. In tumor-bearing mice under chemotherapy, supplementation with fish oil and selenium prevented a rise in IL-6, TNF-α and myostatin and muscle atrophy. The findings presented here allow us to better understand the molecular basis of cancer cachexia and potentiate nutrition supplementation in future cancer chemotherapy. https://greenmedinfo.com/article/chemotherapy-inhibited-tumor-growth-promoted-cachexia-was-attenuated-combinati#comments Cachexia Cachexia: Chemotherapy Induced Fish Oil Muscle Atrophy Selenium Chemotherapeutic Chemotherapy Interleukin-6 Downregulation Tumor Necrosis Factor (TNF) Alpha Inhibitor Animal Study Sat, 02 May 2015 22:13:10 +0000 greenmedinfo 117081 at https://greenmedinfo.com Chemotherapy-induced cachexia dysregulates hypothalamic and systemic lipoamines and is attenuated by cannabigerol. https://greenmedinfo.com/article/chemotherapy-induced-cachexia-dysregulates-hypothalamic-and-systemic-lipoamine PMID:  J Cachexia Sarcopenia Muscle. 2019 Aug ;10(4):844-859. Epub 2019 Apr 29. PMID: 31035309 Abstract Title:  Chemotherapy-induced cachexia dysregulates hypothalamic and systemic lipoamines and is attenuated by cannabigerol. Abstract:  BACKGROUND: Muscle wasting, anorexia, and metabolic dysregulation are common side-effects of cytotoxic chemotherapy, having a dose-limiting effect on treatment efficacy, and compromising quality of life and mortality. Extracts of Cannabis sativa, and analogues of the major phytocannabinoidΔ9-tetrahydrocannabinol, have been used to ameliorate chemotherapy-induced appetite loss and nausea for decades. However, psychoactive side-effects limit their clinical utility, and they have little efficacy against weight loss. We recently established that the non-psychoactive phytocannabinoid cannabigerol (CBG) stimulates appetite in healthy rats, without neuromotor side-effects. The present study assessed whether CBG attenuates anorexia and/or other cachectic effects induced by the broad-spectrum chemotherapy agent cisplatin.METHODS: An acute cachectic phenotype was induced in adult male Lister-hooded rats by 6 mg/kg (i.p.) cisplatin. In total 66 rats were randomly allocated to groups receiving vehicle only, cisplatin only, or cisplatin and 60 or 120 mg/kg CBG (po, b.i.d.). Feeding behavior, bodyweight and locomotor activity were recorded for 72 hours, at which point rats were sacrificed for post-mortem analyses. Myofibre atrophy, protein synthesis and autophagy dysregulation were assessed in skeletal muscle, plasma metabolic profiles were obtained by untargeted 1H-NMR metabonomics, and levels of endocannabinoid-like lipoamines quantified in plasma and hypothalami by targeted HPLC-MS/MS lipidomics.RESULTS: CBG (120 mg/kg) modestly increased food intake, predominantly at 36-60hrs (p<p><a href="https://greenmedinfo.com/article/chemotherapy-induced-cachexia-dysregulates-hypothalamic-and-systemic-lipoamine" target="_blank">read more</a></p> https://greenmedinfo.com/article/chemotherapy-induced-cachexia-dysregulates-hypothalamic-and-systemic-lipoamine#comments Cachexia: Chemotherapy Induced Cannabigerol Anti-Cachexic Agents Animal Study Tue, 17 Sep 2019 01:25:35 +0000 greenmedinfo 196611 at https://greenmedinfo.com Chemotherapy-induced loss of bone and muscle mass in a mouse model of breast cancer bone metastases and cachexia. https://greenmedinfo.com/article/chemotherapy-induced-loss-bone-and-muscle-mass-mouse-model-breast-cancer-bone- PMID:  JCSM Rapid Commun. 2019 Jan-Jun;2(1). PMID: 31032492 Abstract Title:  Chemotherapy-induced loss of bone and muscle mass in a mouse model of breast cancer bone metastases and cachexia. Abstract:  Background: Chemotherapy used to treat malignancy can lead to loss of skeletal muscle mass and reduced force production, and can reduce bone volume in mice. We have shown that bone-muscle crosstalk is a key nexus in skeletal muscle function and bone homeostasis in osteolytic breast cancer bone metastases. Because chemotherapy has significant negative side effects on bone mass, and because bone loss can drive skeletal muscle weakness, we have examined the effects of chemotherapy on the musculoskeletal system in mice with breast cancer bone metastases.Methods and results: Six-week-old Female athymic nude mice were inoculated with 10MDA-MB231 human breast cancer cells into the left ventricle and bone metastases were confirmed by X-ray. Mice were injected with carboplatin at a dose of 60mg/kg once per week starting 4 days after tumor inoculation. Skeletal muscle was collected for biochemical analysis and extensor digitorum longus (EDL) whole muscle contractility was measured. The femur and tibia bone parameters were assessed by microCT and tumor burden in bone was determined by histology. Healthy mice treated with carboplatin lose whole body weight and have reduced individual muscle weights (gastrocnemius, tibialis anterior (TA), and EDL), reduced trabecular bone volume (BV/TV), and reduced EDL function. Mice with MDA-MB-231 bone metastases treated with carboplatin lose body weight, and have reduced EDL function as healthy mice treated with carboplatin. Mice with MDA-MB-231 bone metastases plus carboplatin do have reduced proximal tibia BV/TV compared to carboplatin alone, but carboplatin does reduce tumor burden in bone.Conclusions: Our data shows that carboplatin treatment, aimed at reducing tumor burden, contributes to cachexia and trabecular bone loss. The muscle atrophy and weakness may occur through bone-muscle crosstalk and would lead to a feed-forward cycle of musculoskeletal degradation. Despite anti-tumor effects of chemotherapy, musculoskeletal impairment is still significant in mice with bone metastases. <p><a href="https://greenmedinfo.com/article/chemotherapy-induced-loss-bone-and-muscle-mass-mouse-model-breast-cancer-bone-" target="_blank">read more</a></p> https://greenmedinfo.com/article/chemotherapy-induced-loss-bone-and-muscle-mass-mouse-model-breast-cancer-bone-#comments Breast Cancer Cachexia: Chemotherapy Induced Animal Study Tue, 08 Oct 2019 18:39:25 +0000 greenmedinfo 198421 at https://greenmedinfo.com Low molecular weight fucoidan is a potential agent for preventing cancer cachexia-associated muscle atrophy during chemotherapy. https://greenmedinfo.com/article/low-molecular-weight-fucoidan-potential-agent-preventing-cancer-cachexia-assoc PMID:  Oncotarget. 2016 Jun 13. Epub 2016 Jun 13. PMID: 27323407 Abstract Title:  Combined administration of fucoidan ameliorates tumor and chemotherapy-induced skeletal muscle atrophy in bladder cancer-bearing mice. Abstract:  Cancer cachexia is characterized by anorexia, skeletal muscle atrophy, and systemic inflammation. Fucoidan extracted from brown algae exhibits anti-inflammatory and anticancer activities. However, whether fucoidan ameliorates tumour and chemotherapy-induced muscle atrophy and -related cachectic symptoms remains unknown. Compared with mice with bladder cancer treated with chemotherapy alone (TGC group), those treated with a combination of low molecular weight fucoidan (LMWF) and chemotherapy drugs such as gemcitabine and cisplatin (TGCF) showed a significant reduction of body weight loss, muscle atrophy, and intestinal injury and dysfunction. Moreover, myostatin, activin A, and pro-inflammatory cytokine production, FoxO3 expression and activation, NF-κB activation, MuRF-1 and MAFbx/atrogin-1 expression, and proteasome activity in muscle were significantly decreased in the TGCF group compared with the TGC group. In addition, insulin-like growth factor 1 (IGF-1) expression and formation, and IGF-1-regulated mTOR/p70S6k/4EBP-1 protein synthesis signalling were elevated in the TGCF group compared with the TGC group. Taken together, these results suggest that LMWF is a potential agent for preventing cancer cachexia-associated muscle atrophy during chemotherapy. Furthermore, the beneficial effect of LMWF may be attributed to suppressing NF-κB-evoked inflammation, myostatin and activin A production, and subsequent muscle proteolysis, and enhancing IGF-1-dependent protein synthesis. <p><a href="https://greenmedinfo.com/article/low-molecular-weight-fucoidan-potential-agent-preventing-cancer-cachexia-assoc" target="_blank">read more</a></p> https://greenmedinfo.com/article/low-molecular-weight-fucoidan-potential-agent-preventing-cancer-cachexia-assoc#comments Bladder Cancer Cachexia: Chemotherapy Induced Fucoidan Anti-Cachexic Agents Anti-Inflammatory Agents NF-kappaB Inhibitor Animal Study Tue, 13 Dec 2016 22:49:22 +0000 greenmedinfo 140391 at https://greenmedinfo.com Magnolol is a promising chemopreventive supplement for preventing chemotherapy-induced skeletal muscle atrophy associated with cancer cachexia. https://greenmedinfo.com/article/magnolol-promising-chemopreventive-supplement-preventing-chemotherapy-induced- PMID:  PLoS One. 2015 ;10(11):e0143594. Epub 2015 Nov 24. PMID: 26600425 Abstract Title:  Supplementation of Magnolol Attenuates Skeletal Muscle Atrophy in Bladder Cancer-Bearing Mice Undergoing Chemotherapy via Suppression of FoxO3 Activation and Induction of IGF-1. Abstract:  Skeletal muscle atrophy, the most prominent phenotypic feature of cancer cachexia, is often observed in cancer patients undergoing chemotherapy. Magnolol (M) extracted from Magnolia officinalis exhibits several pharmacological effects including anti-inflammatory and anticancer activities. In this study, we investigated whether magnolol supplementation protects against the development of cachexia symptoms in bladder cancer-bearing mice undergoing chemotherapy. Combined treatment of magnolol with chemotherapeutic drugs, such as gemcitabine and cisplatin (TGCM) or gemcitabine (TGM), markedly attenuates the body weight loss and skeletal muscle atrophy compared with conventional chemotherapy (TGC). The antiatrophic effect of magnolol may be associated with inhibition of myostatin and activin A formation, as well as FoxO3 transcriptional activity resulting from Akt activation, thereby suppressing ubiquitin ligases MuRF-1 and MAFbx/atrogin-1 expression, as well as proteasomal enzyme activity. Notably, magnolol-induced insulin-like growth factor 1 (IGF-1) production and related protein synthesis may also contribute to its protective effects. The decreased food intake, and intestinal injury and dysfunction observed in the mice of TGC group were significantly improved in the TGCM and TGM groups. Moreover, the increased inflammatory responses evidenced by elevation of proinflammatory cytokine formation and NF-κB activation occurred in the atrophying muscle of TGC group were markedly inhibited in mice of combined treatment with magnolol. In summary, these findings support that magnolol is a promising chemopreventive supplement for preventing chemotherapy-induced skeletal muscle atrophy associated with cancer cachexia by suppressing muscle protein degradation, and inflammatory responses, as well as increasing IGF-1-mediated protein synthesis. https://greenmedinfo.com/article/magnolol-promising-chemopreventive-supplement-preventing-chemotherapy-induced-#comments Bladder Cancer Cachexia: Cancer Cachexia: Chemotherapy Induced Magnolia Magnolol Anti-Inflammatory Agents NF-kappaB Inhibitor Gene Expression Regulation Animal Study Fri, 04 Dec 2015 01:30:57 +0000 greenmedinfo 122065 at https://greenmedinfo.com Magnolol may be a promising chemoprotective agent for the prevention of muscle atrophy. https://greenmedinfo.com/article/magnolol-may-be-promising-chemoprotective-agent-prevention-muscle-atrophy PMID:  Front Immunol. 2020 ;11:77. Epub 2020 Feb 7. PMID: 32117241 Abstract Title:  Magnolol Attenuates Cisplatin-Induced Muscle Wasting by M2c Macrophage Activation. Abstract:  Cancer chemotherapy induces sarcopenia, which is a rapid loss of muscle mass that directly restricts daily activities and leads to poor quality of life and increased mortality. Although hormone-related therapies have been used to improve appetite and nutritional status, current treatments are considered palliative. Thus, the protection of skeletal muscle loss without adverse effects is essential to allow the maintenance of chemotherapy in cancer patients. Magnolol fromhas several pharmacological effects including anti-cancer and anti-inflammatory activities, but the protection from muscle atrophy is not well-understood. In the present study, we investigated the effects of magnolol on muscle wasting and macrophage subtypes in a cisplatin-induced sarcopenia mouse model. We showed that magnolol significantly attenuated the body weight and the muscle loss induced by cisplatin injection. The diameter of the tibialis anterior muscle was markedly increased after magnolol treatment in cisplatin-treated mice. Importantly, magnolol increased macrophage infiltration into skeletal muscle while not affecting proliferation of macrophages. Magnolol attenuated the imbalance of M1/M2c macrophages by increasing CD206CD163M2c tissue reparative macrophages. Further, magnolol increased insulin-like growth factor (IGF)-1 expression. This effect was also observed in bone marrow-derived macrophages upon magnolol treatment. Taken together, magnolol may be a promising chemoprotective agent for the prevention of muscle atrophy through the upregulating M2c macrophages, which are a major source of IGF-1. <p><a href="https://greenmedinfo.com/article/magnolol-may-be-promising-chemoprotective-agent-prevention-muscle-atrophy" target="_blank">read more</a></p> https://greenmedinfo.com/article/magnolol-may-be-promising-chemoprotective-agent-prevention-muscle-atrophy#comments Cachexia: Chemotherapy Induced Chemotherapy-Induced Toxicity: Cisplatin Magnolol Anti-Cachexic Agents Chemoprotective Agents Animal Study Thu, 26 Mar 2020 06:30:37 +0000 greenmedinfo 217167 at https://greenmedinfo.com Paeonia lactiflora extract suppresses cisplatin-induced muscle wasting. https://greenmedinfo.com/article/paeonia-lactiflora-extract-suppresses-cisplatin-induced-muscle-wasting PMID:  J Ethnopharmacol. 2020 Sep 21:113403. Epub 2020 Sep 21. PMID: 32971160 Abstract Title:  Paeonia lactiflora extract suppresses cisplatin-induced muscle wasting via downregulation of muscle-specific ubiquitin E3 ligases, NF-κB signaling, and cytokine levels. Abstract:  ETHNOPHARMACOLOGICAL RELEVANCE: The dried root of Paeonia lactiflora Pall. (Radix Paeoniae) has been traditionally used to treat various inflammatory diseases in many Asian countries.AIM OF THE STUDY: Cisplatin is a broad-spectrum anticancer drug used in diverse types of cancer. However, muscle wasting is a common side effect of cisplatin chemotherapy. This study aimed to elucidate the effects of an ethanol extract of the root of Paeonia lactiflora Pall. (Radix Paeoniae, RP) on cisplatin-induced muscle wasting along with its molecular mechanism.MATERIAL AND METHODS: C57BL/6 mice were intraperitoneally injected with cisplatin and orally treated with RP. Megestrol acetate was used as a comparator drug. Skeletal muscle mass was measured as the weight of gastrocnemius and quadriceps muscles, and skeletal muscle function was measured by treadmill running time and grip strength. Skeletal muscle tissues were analyzed by RNAseq, western blotting, ELISA, and immunofluorescence microscopy.RESULTS: In mice treated with cisplatin, skeletal muscle mass and skeletal muscle function were significantly reduced. However, oral administration of RP significantly restored skeletal muscle mass and function in the cisplatin-treated mice. In the skeletal muscle tissues of the cisplatin-treated mice, RP downregulated NF-κB signaling and cytokine levels. RP also downregulated muscle-specific ubiquitin E3 ligases, resulting in the restoration of myosin heavy chain (MyHC) and myoblast determination protein (MyoD), which play crucial roles in muscle contraction and muscle differentiation, respectively.CONCLUSION: RP restored skeletal muscle function and mass in cisplatin-treated mice by restoring the muscle levels of MyHC and MyoD proteins via downregulation of muscle-specific ubiquitin E3 ligases as well as muscle NF-κB signaling and cytokine levels. <p><a href="https://greenmedinfo.com/article/paeonia-lactiflora-extract-suppresses-cisplatin-induced-muscle-wasting" target="_blank">read more</a></p> https://greenmedinfo.com/article/paeonia-lactiflora-extract-suppresses-cisplatin-induced-muscle-wasting#comments Cachexia: Chemotherapy Induced Chemotherapy-Induced Toxicity: Cisplatin Peony Anti-Cachexic Agents Chemoprotective Agents NF-kappaB Inhibitor Animal Study Tue, 13 Oct 2020 16:17:41 +0000 greenmedinfo 228038 at https://greenmedinfo.com These findings implicate IL-6 and possibly IGF-1 in the regulation of body composition in breast cancer patients exposed to cytotoxic chemotherapy. https://greenmedinfo.com/article/these-findings-implicate-il-6-and-possibly-igf-1-regulation-body-composition-b PMID:  Biol Res Nurs. 2015 Oct ;17(5):549-57. Epub 2014 Nov 18. PMID: 25406461 Abstract Title:  Induction of IL-6 by Cytotoxic Chemotherapy Is Associated With Loss of Lean Body and Fat Mass in Tumor-free Female Mice. Abstract:  Cancer patients treated with cytotoxic chemotherapy experience fatigue and changes in body composition that can impact physical functioning and quality of life during and after treatment. Interleukin-6 (IL-6) is associated with fatigue in cancer survivors and plays an important role in the regulation of body composition. The purpose of the present study was to determine the specific role of IL-6 in cyclophosphamide-doxorubicin-5-fluorouracil (CAF)-induced changes in fatigue, food intake, and body composition using mice lacking IL-6. Female wild-type (WT) and IL-6 (-/-) mice were injected with four cycles of CAF or normal saline (NS) administered at 21-day intervals. Daily voluntary wheel-running activity (VWRA), used as a proxy for fatigue, and food intake were monitored daily up to 21 days after the fourth dose. Dual-energy X-ray absorptiometry (DEXA) was used to assess treatment-related changes in lean body mass (LBM), fat mass (FM), and bone mineral content (BMC). Patterns of change in fatigue and food intake did not differ between CAF-treated WT and IL-6 (-/-) mice. However, a Genotype× Drug interaction was observed for LBM (p = 0.047) and FM (p = 0.035) but not BMC (p = .569). Whereas WT mice lost LBM and FM during CAF treatment, IL-6-deficient mice did not. Treatment-related decreases in levels of the anabolic hormone insulin-like growth factor-1 (IGF-1) may contribute to LBMand FM loss since CAF decreased IGF-1 levels in an IL-6-dependent manner. These findings implicate IL-6 and possibly IGF-1 in the regulation of body composition in breast cancer patients exposed to cytotoxic chemotherapy. https://greenmedinfo.com/article/these-findings-implicate-il-6-and-possibly-igf-1-regulation-body-composition-b#comments Cachexia: Chemotherapy Induced Inflammation Animal Study Thu, 21 Jan 2016 01:46:36 +0000 greenmedinfo 123317 at https://greenmedinfo.com These results show that ginger extract can be considered a treatment option to alleviate cisplatin-induced anorexia. https://greenmedinfo.com/article/these-results-show-ginger-extract-can-be-considered-treatment-option-alleviate PMID:  Front Pharmacol. 2023 ;14:1267254. Epub 2023 Nov 9. PMID: 38026983 Abstract Title:  The effect of ginger extract on cisplatin-induced acute anorexia in rats. Abstract:  Cisplatin is a platinum-based chemotherapeutic agent widely used to treat various cancers. However, several side effects have been reported in treated patients. Among these, acute anorexia is one of the most severe secondary effects. In this study, a single oral administration of 100 or 500 mg/kg ginger extract (GE) significantly alleviated the cisplatin-induced decrease in food intake in rats. However, these body weight and water intake decreases were reversed in the 100 mg/kg group rats. To elucidate the underlying mechanism of action, serotonin (5-HT) and 5-HT,andreceptors in the nodose ganglion of the vagus nerve were investigated. The results showed that cisplatin-induced increases in serotonin levels in both the blood and nodose ganglion tissues were significantly decreased by100 and 500 mg/kg of GE administration. On 5-HT receptors, 5-HTand, but notreceptors, were affected by cisplatin, and GE 100 and 500 mg/kg succeeded in downregulating the evoked upregulated gene of these receptors. Protein expression of 5-HTandreceptors were also reduced in the 100 mg/kg group. Furthermore, the injection of 5-HTandreceptors antagonists (palonostron, 0.1 mg/kg, i.p.; piboserod, 1 mg/kg, i.p., respectively) in cisplatin treated rats prevented the decrease in food intake. Using high-performance liquid chromatography (HPLC) analysis, [6]-gingerol and [6]-shogaol were identified and quantified as the major components of GE, comprising 4.12% and 2.15% of the GE, respectively. Although [6]-gingerol or [6]-shogaol alone failed to alleviate the evoked anorexia, when treated together, the effect was significant on the cisplatin-induced decrease in food intake. These results show that GE can be considered a treatment option to alleviate cisplatin-induced anorexia. <p><a href="https://greenmedinfo.com/article/these-results-show-ginger-extract-can-be-considered-treatment-option-alleviate" target="_blank">read more</a></p> https://greenmedinfo.com/article/these-results-show-ginger-extract-can-be-considered-treatment-option-alleviate#comments Anorexia: Cancer-Associated Cachexia: Chemotherapy Induced Chemotherapy-Induced Toxicity: Cisplatin Ginger Anti-Cachexic Agents Chemoprotective Agents Animal Study Fri, 01 Mar 2024 01:56:27 +0000 greenmedinfo 288983 at https://greenmedinfo.com