Drug-Induced Toxicity: Gastrointestinal https://greenmedinfo.com/taxonomy/term/41571/all en A. senticosus polysaccharide has an obvious protective effect on the gut homeostasis of Drosophila melanogaster. https://greenmedinfo.com/article/senticosus-polysaccharide-has-obvious-protective-effect-gut-homeostasis-drosop PMID:  Phytother Res. 2020 Jan ;34(1):193-200. Epub 2019 Nov 17. PMID: 31736181 Abstract Title:  Acanthopanax senticosus polysaccharide regulates the intestinal homeostasis disruption induced by toxic chemicals in Drosophila. Abstract:  The intestinal epithelium provides the first line of defense against pathogens and toxic compounds. The ingestion of toxic compounds causes an enhanced epithelial cell death and an excessive proliferation of intestinal stem cells, eventually resulting in the disruption of gut homeostasis. In this study, Drosophila gut inflammation model induced by toxic compounds was exploited to analyze the ameliorative effect of Acanthopanax senticosus polysaccharide on the disruption of gut homeostasis. As a result, it was found that A. senticosus polysaccharide can significantly increase the survival rate of Drosophila adults as well as reduce the excessive proliferation and differentiation of intestinal stem cells through epidermal growth factor receptor, jun-N-terminal kinase, and Notch signaling pathways under the exposure totoxic compounds dextran sodium sulfate. Moreover, the polysaccharide effectively decreased the epithelial cell death and the accumulation of reactive oxygen species and antimicrobial peptides induced by sodium dodecyl sulfate. In addition, it was found that A. senticosus polysaccharide can extendthe lifespan of only female flies but not male flies. In conclusion, A. senticosus polysaccharide has an obvious protective effect on the gut homeostasis of Drosophila melanogaster. <p><a href="https://greenmedinfo.com/article/senticosus-polysaccharide-has-obvious-protective-effect-gut-homeostasis-drosop" target="_blank">read more</a></p> https://greenmedinfo.com/article/senticosus-polysaccharide-has-obvious-protective-effect-gut-homeostasis-drosop#comments Drug-Induced Toxicity: Gastrointestinal Ginseng (Siberian) Gastrointestinal Agents Gastroprotective Insect Study Sun, 26 Jan 2020 14:53:36 +0000 greenmedinfo 209337 at https://greenmedinfo.com Alendronate is associated with injury and ulceration of the gastric mucosa. https://greenmedinfo.com/article/alendronate-associated-injury-and-ulceration-gastric-mucosa PMID:  Aliment Pharmacol Ther. 2000 Nov;14(11):1451-7. PMID: 11069316 Abstract Title:  A randomized controlled trial to assess alendronate-associated injury of the upper gastrointestinal tract. Abstract:  BACKGROUND: Aminobisphosphonates are recommended for postmenopausal osteoporosis but have been associated with injury to the upper gastrointestinal tract. AIM: To conduct a randomized controlled trial, to assess the endoscopic damage caused by alendronate and its effect on gastric mucosal prostaglandin synthesis. METHODS: Seventy-six healthy volunteers age 40-60 years, with normal baseline endoscopy were randomly assigned to treatment with: (A) ASA 650 mg q. d.s.; (B) alendronate 10 mg o.d.; or (C) placebo o.d. for 14 days. Mucosal injury scores on day 14 of treatment were reported by a blinded endoscopist. Gastric biopsies were analysed for prostaglandin E2 (PGE2) concentration by radioimmunoassay. RESULTS: Oesophageal injury did not differ among treatment groups. Gastric ulcers developed in five out of 26 subjects given ASA, two out of 25 given alendronate, and none of 25 given placebo. The mucosal damage scores for the alendronate group exceeded those for the placebo group in the gastric body but not at other sites. Injury scores for ASA exceeded those for placebo in the duodenum, antrum, body, and fundus. The mean change in log10[PGE2] (ng/mg protein) was - 0.07 for placebo, - 0.80 for ASA, and + 0.62 for alendronate (differences not significant). CONCLUSIONS: Alendronate is associated with injury and ulceration of the gastric mucosa. This effect was not associated with any significant change in gastric mucosal PGE2 levels. https://greenmedinfo.com/article/alendronate-associated-injury-and-ulceration-gastric-mucosa#comments Drug-Induced Toxicity: Gastrointestinal Gastric Ulcer Osteoporosis Alendronate (trade name Fosamax) Aspirin Gastrotoxic Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Ulcerogenic Human Study Tue, 09 Nov 2010 23:03:43 +0000 greenmedinfo 58542 at https://greenmedinfo.com Alpha-lipoic acid: A promising adjuvant for nonsteroidal anti-inflammatory drugs therapy with improved efficacy and gastroprotection. https://greenmedinfo.com/article/alpha-lipoic-acid-promising-adjuvant-nonsteroidal-anti-inflammatory-drugs-ther PMID:  Drug Dev Res. 2021 Jan 24. Epub 2021 Jan 24. PMID: 33491260 Abstract Title:  Alpha-lipoic acid: A promising adjuvant for nonsteroidal anti-inflammatory drugs therapy with improved efficacy and gastroprotection. Abstract:  Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used in a wide variety of diseases due to their analgesic and anti-inflammatory effects, but their usage have been limited due to significant ulcerogenic side effects. In the present study, we aimed to evaluate the effect ofα-lipoic acid (ALA) treatment on the anti-inflammatory activity of indomethacin (Indo) as well as the possible therapeutic effect of ALA on high dose Indo-induced gastropathy in female mice. Mice were treated with Indo (5 or 30 mg/kg, p.o) alone or in combination with ALA (50, 100 or 200 mg/kg,i.p). in vivo anti-inflammatory effect was evaluated by formalin-induced paw edema measured as paw thickness and edema. Gastric damage was evaluated macroscopically and histologically by scoring mucosal hemorrhage, erosion, edema and inflammation. To our results, Indo was ineffective at 5 mg/kg, but co-treatment with Indo and ALA significantly reduced paw edema, implying that ALA augmented the anti-inflammatory effect of subtherapeutic dose of Indo. However, ALA was not able to induce a further increase in the anti-inflammatory effect of Indo at 30 mg/kg. Unlike the treatment with Indo at 5mg/kg, Indo at 30 mg/kg caused severe gastric damage that prevented by co-treatment with ALA. These results suggest that combination of ALA with NSAIDs can both increase anti-inflammatory effect and prevent NSAIDs-induced gastric damage. ALA would be promising adjuvant that can reduce dose for effective NSAID therapy, which improves safety profile of NSAIDs especially in cases long-term administration of high dose needed. <p><a href="https://greenmedinfo.com/article/alpha-lipoic-acid-promising-adjuvant-nonsteroidal-anti-inflammatory-drugs-ther" target="_blank">read more</a></p> https://greenmedinfo.com/article/alpha-lipoic-acid-promising-adjuvant-nonsteroidal-anti-inflammatory-drugs-ther#comments Alpha-Lipoic Acid Drug-Induced Toxicity: Gastrointestinal Inflammation Gastroprotective Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Animal Study Sat, 27 Mar 2021 22:00:38 +0000 greenmedinfo 236989 at https://greenmedinfo.com Berberine ameliorates NSAIDs-induced intestinal injury by the repair of enteric nervous system. https://greenmedinfo.com/article/berberine-ameliorates-nsaids-induced-intestinal-injury-repair-enteric-nervous- PMID:  Fundam Clin Pharmacol. 2019 Sep 13. Epub 2019 Sep 13. PMID: 31520444 Abstract Title:  Berberine ameliorates NSAIDs-induced intestinal injury by the repair of enteric nervous system. Abstract:  The study was to detect the role of GDNF, PGP9.5 (a neuronal marker) and GFAP (EGCs&#039; marker) in the mechanism of NSAIDs related to intestinal injury, and to clarify the protective effect of berberine in the treatment of NSAID-induced small intestinal disease. 40 males SD rats were divided randomly into five groups (A-E): Group A: control group; Group B: model group received diclofenac sodium 7.5mg/(kg*d) for five days; Group C,D,E: berberine low, medium and high dose groups were treated by 7.5mg/(kg*d) diclofenac sodium for five days then received berberine 25mg/(kg*d) ,50mg/(kg*d), 75mg/(kg*d) respectively, between the sixth and eighth day. Intestinal mucosa was taken on the ninth day to observe the general, histological injuries, and to measure the intestinal epithelial thickness. Then, immunohistochemistry was performed to detect the expression of PGP9.5 and GFAP, and Western blot was performed to detect GDNF expression. The histological score and the general score in the model group were respectively 5.75±1.04 and 4.83±0.92. Scores in berberine medium and high berberine group were lower compared with the model group (P<p><a href="https://greenmedinfo.com/article/berberine-ameliorates-nsaids-induced-intestinal-injury-repair-enteric-nervous-" target="_blank">read more</a></p> https://greenmedinfo.com/article/berberine-ameliorates-nsaids-induced-intestinal-injury-repair-enteric-nervous-#comments Berberine Drug-Induced Toxicity: Gastrointestinal Gastroprotective Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Animal Study Thu, 19 Sep 2019 23:05:54 +0000 greenmedinfo 196775 at https://greenmedinfo.com Bisphosphonates cause mucosal injury to the upper gastrointestinal tract similar to aspirin. https://greenmedinfo.com/article/bisphosphonates-cause-mucosal-injury-upper-gastrointestinal-tract-similar-aspi PMID:  Am J Gastroenterol. 1997 Aug;92(8):1322-5. PMID: 9260798 Abstract Title:  Primary amino-bisphosphonates: a new class of gastrotoxic drugs--comparison of alendronate and aspirin. Abstract:  BACKGROUND: Alendronate and pamidronate are primary amino-bisphosphonates used in the treatment of metabolic bone disease. Both drugs have been associated with reversible erosive esophagitis and as a result pamidronate is approved in the United States only for parenteral use. In rats, alendronate causes acute gastric mucosal damage similar to that seen with aspirin or nonsteroidal anti-inflammatory drugs. METHODS: We performed a blinded, crossover, randomized, single-center, placebo-controlled, endoscopic comparison of alendronate (40 mg/day), aspirin (1, 300 mg/day), and placebo to evaluate the presence and degree of mucosal damage to the esophagus, stomach, and duodenal bulb. RESULTS: Twelve normal healthy volunteers were studied both before and after 4 days of drug therapy. Placebo caused no visible endoscopic damage. In contrast, both aspirin and alendronate were associated with visible gastric mucosal injury in the majority of those studied (75 and 58%, respectively) and both were significantly greater than placebo (p https://greenmedinfo.com/article/bisphosphonates-cause-mucosal-injury-upper-gastrointestinal-tract-similar-aspi#comments Drug-Induced Toxicity: Gastrointestinal Gastric Ulcer Alendronate (trade name Fosamax) Aspirin Gastrotoxic Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Pamidronate Ulcerogenic Human Study Tue, 09 Nov 2010 23:02:54 +0000 greenmedinfo 58541 at https://greenmedinfo.com Bisphosphonates may induce gastrointestinal damage through the inhibition of the mevalonate pathway. https://greenmedinfo.com/article/bisphosphonates-may-induce-gastrointestinal-damage-through-inhibition-mevalona PMID:  Bone. 2001 Oct;29(4):336-43. PMID: 11595616 Abstract Title:  Nitrogen-containing bisphosphonates induce apoptosis of Caco-2 cells in vitro by inhibiting the mevalonate pathway: a model of bisphosphonate-induced gastrointestinal toxicity. Abstract:  Bisphosphonates have become an important addition to the pharmacological armamentarium against postmenopausal osteoporosis. One of the major side effects of oral therapy with some nitrogen-containing bisphosphonates appears to be gastrointestinal (GI) intolerability, particularly esophageal irritation and ulceration. Because nitrogen-containing bisphosphonates can cause apoptosis in a variety of cell types in vitro, by inhibiting the mevalonate pathway, we hypothesized that the effect of these agents on the GI tract may be due to apoptosis or inhibition of growth of gut epithelial cells. A comparison between clodronate, etidronate, pamidronate, alendronate, and risedronate demonstrated that only the nitrogen-containing bisphosphonates were effective at inducing apoptosis or inhibiting proliferation of Caco-2 human epithelial cells in vitro, at concentrations of between 10 and 1000 micromol/L. The ability of nitrogen-containing bisphosphonates to cause apoptosis and inhibit Caco-2 cell proliferation was due to inhibition of the mevalonate pathway, because the addition of farnesol, oxidized low-density lipoprotein (LDL) cholesterol, or especially geranylgeraniol suppressed the effects. Furthermore, pamidronate, alendronate, and risedronate inhibited protein prenylation in Caco-2 cells, as determined by analysis of the processing of Rap1A, a prenylated small GTPase. These studies suggest that the effects of nitrogen-containing bisphosphonates observed in the GI tract may be due to inhibition of proliferation or apoptosis of gut epithelial cells, following loss of prenylated proteins and sterols. https://greenmedinfo.com/article/bisphosphonates-may-induce-gastrointestinal-damage-through-inhibition-mevalona#comments Drug-Induced Toxicity: Gastrointestinal Gastrointestinal Diseases Apoptotic Bisphosphonates Mevalonate Pathway Inhibition In Vitro Study Tue, 09 Nov 2010 22:55:59 +0000 greenmedinfo 58535 at https://greenmedinfo.com Low amounts of dietary fiber may decrease gastrointestinal side-effects associated with the use of NSAIDs. https://greenmedinfo.com/article/low-amounts-dietary-fiber-may-decrease-gastrointestinal-side-effects-associate PMID:  J Physiol Pharmacol. 2016 Aug ;67(4):563-573. PMID: 27779477 Abstract Title:  Diets with no or low amounts of dietary fiber can reduce small intestinal ulcers induced by non-steroidal anti-inflammatory drugs in dogs. Abstract:  Recent progress in endoscopic techniques has revealed that non-steroidal anti-inflammatory drugs (NSAIDs) often cause ulcers in the small intestine in humans, but effective therapy is not available at present. In the present study, we investigated the effects of feeding condition and the amount of dietary fiber (DF) in the diet on the formation of gastrointestinal ulcers induced by NSAIDs in dogs. Several types of diets containing various percentages of DF were given to dogs. Indomethacin (1 or 3 mg/kg, p.o.), ketoprofen (2 mg/kg, s.c.), or fulnixin (1 mg/kg, s.c.) was administered once daily at 10 a.m. after a morning meal or without a morning meal (fasted condition) for 3 - 7 days. Gastrointestinal lesions were examined 24 h after the final dose of the drugs. When indomethacin (3 mg/kg) was administered after a morning meal (fed condition) for 7 days, it produced many lesions in the small intestine. However, when it was given in the fasted condition without the morning meal, the lesions were markedly decreased. All the NSAIDs given after feeding of regular dry food containing 6% DF once a day for 3 days produced many lesions in the small intestine. The lesions were decreased or increased in dogs given prescription diets containing low DF (1.1%) and high DF (15.4%), respectively. Furthermore, lesions were not observed in dogs given canned diet containing very low DF (<p><a href="https://greenmedinfo.com/article/low-amounts-dietary-fiber-may-decrease-gastrointestinal-side-effects-associate" target="_blank">read more</a></p> https://greenmedinfo.com/article/low-amounts-dietary-fiber-may-decrease-gastrointestinal-side-effects-associate#comments Drug-Induced Toxicity: Gastrointestinal Gastroprotective Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Animal Study Tue, 01 Nov 2016 18:01:19 +0000 greenmedinfo 138696 at https://greenmedinfo.com Low molecular weight fucoidan ameliorating the chronic cisplatin-induced delayed gastrointestinal motility in rats. https://greenmedinfo.com/article/low-molecular-weight-fucoidan-ameliorating-chronic-cisplatin-induced-delayed-g PMID:  Food Chem Toxicol. 2012 Dec ;50(12):4468-78. Epub 2012 Sep 25. PMID: 23022014 Abstract Title:  Low molecular weight fucoidan ameliorating the chronic cisplatin-induced delayed gastrointestinal motility in rats. Abstract:  Delayed gastrointestinal (GI) motility is frequent adverse effect associated with chemotherapy due to oxidative stress, activation of 5-HT3 receptors or serotonin releases from enterochromaffin cells. Fucoidan, extracts from brown seaweeds, has been showed antioxidant related favorable pharmacological activities including digestive tract protective effects. Low molecular weight fucoidan (LMF) obtained by acid hydrolysis of high molecular weight fucoidan has been showed more favorable bioactivities. This study was conducted to determine whether or not LMF can prevent delayed GI motility induced by the antineoplastic drug cisplatin chronically administered, once per week for five consecutive weeks. LMF ameliorating the chronic cisplatin treatment related body weight decreases, delayed GI motility, and enhanced the antioxidant defense systems. In addition, LMF also inhibited the cisplatin treatment related GI gastrin and serotonin changes, including enzyme activities involved in serotonin metabolism and enterochromaffin cells. The overall effects of LMF 10mg/kg were similar to that of ondansetron 1mg/kg, a serotonin 5-HT3 receptor antagonist. The present results supported that LMF have favorable ameliorating effect on the delayed GI motility induced by chemotherapy, modulated the GI enterochromaffin cells, serotonin and gastrin-producing cells with antioxidant effects. This effect of LMF may help improve accompanying digestive disorders by chemotherapy. https://greenmedinfo.com/article/low-molecular-weight-fucoidan-ameliorating-chronic-cisplatin-induced-delayed-g#comments Chemotherapy-Induced Toxicity: Cisplatin Drug-Induced Toxicity: Gastrointestinal Fucoidan Animal Study Fri, 07 Dec 2012 16:08:57 +0000 greenmedinfo 86270 at https://greenmedinfo.com Luteolin prevents intestinal mucositis induced by irinotecan. https://greenmedinfo.com/article/luteolin-prevents-intestinal-mucositis-induced-irinotecan PMID:  Br J Pharmacol. 2020 Jan 24. Epub 2020 Jan 24. PMID: 31976547 Abstract Title:  Luteolin prevents irinotecan-induced intestinal mucositis in mice through antioxidant and anti-inflammatory properties. Abstract:  BACKGROUND AND PURPOSE: Intestinal mucositis refers to mucosal damage caused by cancer treatment and irinotecan is one of the agents most associated with this condition. Focusing on the development of alternatives to prevent this important adverse effect, we evaluated the activity of the flavonoid luteolin, which has never been tested for this purpose despite its biological potential.EXPERIMENTAL APPROACH: The effects of luteolin were examined on irinotecan-induced intestinal mucositis in mice. Clinical signs were evaluated. Moreover, histological, oxidative and inflammatory parameters were analyzed, as well as the possible interference of luteolin in the antitumor activity of irinotecan.KEY RESULTS: Luteolin at 30 mg/kg (p.o. or i.p), prevents irinotecan-induced intestinal damage by reducing weight loss and diarrhea score and attenuating the shortening of the duodenum and colon. The histological analysis confirmed that luteolin (30 mg/kg, p.o.) prevented villous shortening, vacuolization, and apoptosis of cells and preserved mucin production in the duodenum and colon. Moreover, luteolin treatment mitigated irinotecan-induced oxidative stress (i.e. by reducing the levels of ROS and LOOH, and augmenting endogenous antioxidants) and inflammation (i.e. through the decrease of MPO enzyme activity, TNF, IL-1β, and IL-6 levels; and increasing IL-4 and IL-10). Besides, the disruption of the tight junctions ZO-1 and occludin were also prevented by luteolin treatment. Importantly, luteolin did not interfere with the antitumor activity of irinotecan.CONCLUSION AND IMPLICATIONS: Luteolin prevents intestinal mucositis induced by irinotecan and therefore could be a potential adjunct in antitumor therapy to control this adverse effect, increasing treatment adherence and consequently the chances of cancer remission. <p><a href="https://greenmedinfo.com/article/luteolin-prevents-intestinal-mucositis-induced-irinotecan" target="_blank">read more</a></p> https://greenmedinfo.com/article/luteolin-prevents-intestinal-mucositis-induced-irinotecan#comments Chemotherapy-Induced Toxicity: Irinotecan Drug-Induced Toxicity: Gastrointestinal Luteolin Mucositis Anti-Inflammatory Agents Chemoprotective Agents Gastroprotective Interleukin-1 beta downregulation Interleukin-10 upregulation Interleukin-4 upregulation Interleukin-6 Downregulation Irinotecan Tumor Necrosis Factor (TNF) Alpha Inhibitor Animal Study Sat, 08 Feb 2020 01:36:46 +0000 greenmedinfo 210905 at https://greenmedinfo.com Naringin may become a new method to treat and prevent NSAIDs related intestinal diseases. https://greenmedinfo.com/article/naringin-may-become-new-method-treat-and-prevent-nsaids-related-intestinal-dis PMID:  Life Sci. 2020 Dec 15 ;266:118909. Epub 2020 Dec 15. PMID: 33333047 Abstract Title:  Protective effect of naringin on small intestine injury in NSAIDs related enteropathy by regulating ghrelin/GHS-R signaling pathway. Abstract:  OBJECTIVE: To investigate the mechanism of Ghrelin/GHS-R signaling pathway in small intestine injury induced by NSAIDs related enteropathy. To clarify the mechanism network of intestinal mucosal repair with naringin as a new therapeutic method.METHODS: Naringin was used as the intervention method, observed the damage of small intestinal mucosa and detected the expression of ghrelin, GHS-R, leptin and TNF-α by electron microscopy, HE staining and immunohistochemistry.RESULTS: Compared with the control group, the weight of rats in the model group decreased, the thickness of intestinal mucosa became thinner, the structure of intestinal mucosa changed, the expression of ghrelin, GHS-R and leptin decreased, the expression of TNF-α increased. Compared with the model group, the intestinal mucosa of the treatment group was repaired, the expression of ghrelin, GHS-R and leptin was increased, and the expression TNF-α was decreased.CONCLUSION: The mechanism of intestinal mucosal damage in patients with NSAIDs related enteropathy may be related to the decreased expression of ghrelin, GHS-R and leptin, and promotion of TNF-α secretion. Naringin can effectively promote the secretion of ghrelin and leptin, the expression of GSH-R, and inhibit the release of TNF-α, so as to repair intestinal mucosa naringin will become a new method to treat and prevent NSAIDs related intestinal diseases. <p><a href="https://greenmedinfo.com/article/naringin-may-become-new-method-treat-and-prevent-nsaids-related-intestinal-dis" target="_blank">read more</a></p> https://greenmedinfo.com/article/naringin-may-become-new-method-treat-and-prevent-nsaids-related-intestinal-dis#comments Citrus naringin Drug-Induced Toxicity: Gastrointestinal Anti-Inflammatory Agents Gastrointestinal Agents Gastroprotective Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Tumor Necrosis Factor (TNF) Alpha Inhibitor Animal Study Fri, 01 Jan 2021 00:13:38 +0000 greenmedinfo 232085 at https://greenmedinfo.com Natural polyphenols prevent indomethacin-induced and diclofenac-induced Caco-2 cell death. https://greenmedinfo.com/article/natural-polyphenols-prevent-indomethacin-induced-and-diclofenac-induced-caco-2 PMID:  J Pharm Pharmacol. 2020 Jan 10. Epub 2020 Jan 10. PMID: 31922618 Abstract Title:  Natural polyphenols prevent indomethacin-induced and diclofenac-induced Caco-2 cell death by reducing endoplasmic reticulum stress regardless of their direct reactive oxygen species scavenging capacity. Abstract:  OBJECTIVES: Indomethacin (INDO) and diclofenac (DIC) can induce intestinal cell death through induction of oxidative stress-mediated ER stress and mitochondrial dysfunction. This study investigated the cytoprotective potential of 11 polyphenols, namely caffeic acid (CAF), curcumin (CUR), epigallocatechin gallate (EGCG), gallic acid (GAL), hypophyllanthin (HYPO), naringenin (NAR), phyllanthin (PHY), piperine (PIP), quercetin (QUE), rutin (RUT) and silymarin (SLY) against these two NSAIDs in Caco-2 cells.METHODS: Reactive oxygen species (ROS) production was determined with fluorescence spectroscopy using specific probes (DHE, DCFH-DA, HPF). Cell viability and mitochondrial function were assessed by MTT and TMRE assays. The mRNA levels of Bax, Bcl-2 and CHOP proteins were determined by quantitative real-time polymerase chain reaction technique.KEY FINDINGS: All test polyphenols reduced NSAIDs-mediated ROS production. Only EGCG, QUE and RUT protected INDO-/DIC-induced cell death. These three polyphenols suppressed Bax/Bcl-2 mRNA ratio, CHOP up-regulation and MMP disruption in NSAIDs-treated cells. CAF and NAR prevented cytotoxicity from INDO, but not DIC. The cytoprotective effect of NAR, but not CAF, involved alteration of Bax/Bcl-2 mRNA ratio or MMP disruption, but not CHOP transcription.CONCLUSION: The cytoprotective activity of polyphenols against NSAIDs-induced toxicity stemmed from either suppression of CHOP-related ER and mitochondria stresses or other CHOP-independent pathways, but not from the intrinsic ROS scavenging capacity. <p><a href="https://greenmedinfo.com/article/natural-polyphenols-prevent-indomethacin-induced-and-diclofenac-induced-caco-2" target="_blank">read more</a></p> https://greenmedinfo.com/article/natural-polyphenols-prevent-indomethacin-induced-and-diclofenac-induced-caco-2#comments Caffeic Acid Curcumin Drug-Induced Toxicity: Gastrointestinal Drug-Induced Toxicity: Indomethacin EGCG (Epigallocatechin gallate) Gallic Acid Naringenin Piperine Polyphenols Quercetin Rutin Silymarin Antioxidants Diclofenac Gastroprotective Indomethacin Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) In Vitro Study Mon, 17 Feb 2020 21:44:03 +0000 greenmedinfo 212314 at https://greenmedinfo.com Panax notoginseng saponin attenuates gastric mucosal epithelial cell injury induced by dual antiplatelet drugs. https://greenmedinfo.com/article/panax-notoginseng-saponin-attenuates-gastric-mucosal-epithelial-cell-injury-in PMID:  Chin J Integr Med. 2021 Jan 15. Epub 2021 Jan 15. PMID: 33449280 Abstract Title:  Panax Notoginseng Saponin Attenuates Gastric Mucosal Epithelial Cell Injury Induced by Dual Antiplatelet Drugs through COX and PI3K/Akt/ VEGF-GSK-3β-RhoA Network Pathway. Abstract:  OBJECTIVE: To elucidate the underlying mechanism of Panax notoginseng saponin (PNS) on gastric epithelial cell injury and barrier dysfunction induced by dual antiplatelet (DA).METHODS: Human gastric mucosal epithelial cell (GES-1) was cultured and divided into 4 groups: a control, a DA, a PNS+DA and a LY294002+PNS+DA group. GES-1 apoptosis was detected by flow cytometry, cell permeability were detected using Transwell, level of prostaglandins E2 (PGE2), 6-keto-prostaglandin F1α (6-keto-PGF1α) and vascular endothelial growth factor (VEGF) in supernatant were measured by enzyme linked immunosorbent assay (ELISA), expression of phosphatidylinositide 3-kinase (PI3K), phosphorylated-PI3K (p-PI3K), Akt, phosphorylated-Akt (p-Akt), cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), glycogen synthase kinase-3β (GSK-3β) and Ras homolog gene family member A (RhoA) were measured by Western-blot.RESULTS: DA induced apoptosis and hyper-permeability in GES-1, reduced supernatant level of PGE2, 6-keto-PGF1α and VEGF (P<p><a href="https://greenmedinfo.com/article/panax-notoginseng-saponin-attenuates-gastric-mucosal-epithelial-cell-injury-in" target="_blank">read more</a></p> https://greenmedinfo.com/article/panax-notoginseng-saponin-attenuates-gastric-mucosal-epithelial-cell-injury-in#comments Drug-Induced Toxicity: Gastrointestinal Panax Notoginseng Gastroprotective Animal Study Tue, 02 Mar 2021 23:04:57 +0000 greenmedinfo 235518 at https://greenmedinfo.com The results support AGE antioxidant, anti-inflammatory, and antimicrobial potency reflected by the healing of the gastric tissue damage induced by indomethacin. https://greenmedinfo.com/article/results-support-age-antioxidant-anti-inflammatory-and-antimicrobial-potency-re PMID:  Evid Based Complement Alternat Med. 2014 ;2014:759642. Epub 2014 Apr 30. PMID: 24876878 Abstract Title:  The protective effect of aged garlic extract on nonsteroidal anti-inflammatory drug-induced gastric inflammations in male albino rats. Abstract:  Natural products have long gained wide acceptance among the public and scientific community in the gastrointestinal ulcerative field. The present study explore the potential effects of aged garlic extract (AGE) on indomethacin-(IN-) induced gastric inflammation in male rats. Animals were divided into six groups (n = 8) control group, IN-induced gastric inflammation group via oral single dose (30 mg/kg to fasted rats) two AGE orally administered groups (100 and 200 mg/kg for 30 consecutive days) two AGE orally administered groups to rats pretreated with IN at the same aforementioned doses. The results declared the more potent effect of the higher AGE dose (200 mg/kg) as compared to that of the 100 mg/kg dose in the gastroprotective effects reflected by significant gastric mucosal healing of damage and reduction in the total microbial induced due to indomethacin administration. In addition to the significant effect to normalize the significant increase in malondialdehyde (MDA),myeloperoxidase (MPO), tumor necrosis factor- α (TNF- α ) values, and the significant decrease in the total glutathione (tGSH), superoxide dismutase (SOD), and catalase (CAT) values induced by indomethacin. The results support AGE antioxidant, anti-inflammatory, and antimicrobial potency reflected by the healing of the gastric tissue damage induced by indomethacin. https://greenmedinfo.com/article/results-support-age-antioxidant-anti-inflammatory-and-antimicrobial-potency-re#comments Drug-Induced Toxicity: Gastrointestinal Drug-Induced Toxicity: Indomethacin Garlic: Aged Gastrointestinal Inflammation Anti-Inflammatory Agents Antimicrobial Antioxidants Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Plant Extracts Animal Study Sat, 25 Jul 2015 01:46:30 +0000 greenmedinfo 119365 at https://greenmedinfo.com These findings validate the use of Black seed in gastropathies induced by necrotizing agents. https://greenmedinfo.com/article/these-findings-validate-use-black-seed-gastropathies-induced-necrotizing-agent PMID:  Saudi J Gastroenterol. 2008 Jul ;14(3):128-34. PMID: 19568521 Abstract Title:  Gastroprotective effect of an aqueous suspension of black cumin Nigella sativa on necrotizing agents-induced gastric injury in experimental animals. Abstract:  BACKGROUND/AIM: Previous studies on&quot;Black seed&quot;or&quot;Black Cumin&quot;Nigella sativa (NS) have reported a large number of pharmacological activities including its anti-ulcer potential. These studies employed either fixed oil, volatile oil components or different solvent extracts. In folkloric practices, NS seeds are taken as such, in the form of coarse dry powder or the powdered seeds are mixed with water. This study examines the effect of NS aqueous suspension on experimentally induced gastric ulcers and basal gastric secretion in rats to rationalize its use by herbal and Unani medicine practitioners.MATERIALS AND METHODS: The study was conducted at the Medicinal, Aromatic and Poisonous Plants Research Center, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia. Acute gastric ulceration was produced by various noxious chemicals (80% ethanol, 0.2 M NaOH, 25% NaCl and indomethacin) in Wistar albino rats. Anti-secretory studies were undertaken in a separate group of rats. Gastric wall mucus contents and non-protein sulfhydryl concentration were estimated, and gastric tissue was examined histopathologically.RESULTS: An aqueous suspension of Black seed significantly prevented gastric ulcer formation induced by necrotizing agents. It also significantly ameliorated the ulcer severity and basal gastric acid secretion in pylorus-ligated Shay rats. Moreover, the suspension significantly replenished the ethanol-induced depleted gastric wall mucus content levels and gastric mucosal non-protein sulfhydryl concentration. The anti-ulcer effect was further confirmed histopathologically.CONCLUSION: These findings validate the use of Black seed in gastropathies induced by necrotizing agents. The anti-ulcer effect of NS is possibly prostaglandin-mediated and/or through its antioxidant and anti-secretory activities. <p><a href="https://greenmedinfo.com/article/these-findings-validate-use-black-seed-gastropathies-induced-necrotizing-agent" target="_blank">read more</a></p> https://greenmedinfo.com/article/these-findings-validate-use-black-seed-gastropathies-induced-necrotizing-agent#comments Drug-Induced Toxicity: Gastrointestinal Nigella sativa (aka Black Seed) Anti-Ulcer Agents Antioxidants Gastroprotective Animal Study Thu, 27 Apr 2017 21:10:44 +0000 greenmedinfo 146915 at https://greenmedinfo.com