Abstract:Ganoderma lucidum (LEYSS, ex FR., G. lucidum) KARST has been prescribed to improve health and longevity in the traditional Chinese medicine, and it was used for the treatment of neurasthenia, hypertension, hepatopathy and carcinoma for thousands of years.1) More than one hundred species of bioactive components have been isolated from G. lucidum,2) such as polysaccharides, triterpenoids and alkaloids, in which that Ganoderma lucidum polysaccharide (GLPS) is one of the major active components. Its multiple pharm… Show more
“…As previously demonstrated, polysaccharides isolated from G. lucidum , induced total P450 levels in rat liver, whereas suppressed the activity of CYP1A2, CYP3A and CYP2E1 in hepatic microsomes [41]. Our results indicate that GLT is able to induce XRE/AhR and PXR which regulate expression of CYP1A2 and CYP3A, respectively.…”
BackgroundEpidemiological studies suggest that mushroom intake is inversely correlated with gastric, gastrointestinal and breast cancers. We have recently demonstrated anticancer and anti-inflammatory activity of triterpene extract isolated from mushroom Ganoderma lucidum (GLT). The aim of the present study was to evaluate whether GLT prevents colitis-associated carcinogenesis in mice.Methods/Principal FindingsColon carcinogenesis was induced by the food-borne carcinogen (2-Amino-1-methyl-6-phenylimidazol[4,5-b]pyridine [PhIP]) and inflammation (dextran sodium sulfate [DSS]) in mice. Mice were treated with 0, 100, 300 and 500 mg GLT/kg of body weight 3 times per week for 4 months. Cell proliferation, expression of cyclin D1 and COX-2 and macrophage infiltration was assessed by immunohistochemistry. The effect of GLT on XRE/AhR, PXR and rPXR was evaluated by the reporter gene assays. Expression of metabolizing enzymes CYP1A2, CYP3A1 and CYP3A4 in colon tissue was determined by immunohistochemistry. GLT treatment significantly suppressed focal hyperplasia, aberrant crypt foci (ACF) formation and tumor formation in mice exposed to PhIP/DSS. The anti-proliferative effects of GLT were further confirmed by the decreased staining with Ki-67 in colon tissues. PhIP/DSS-induced colon inflammation was demonstrated by the significant shortening of the large intestine and macrophage infiltrations, whereas GLT treatment prevented the shortening of colon lengths, and reduced infiltration of macrophages in colon tissue. GLT treatment also significantly down-regulated PhIP/DSS-dependent expression of cyclin D1, COX-2, CYP1A2 and CYP3A4 in colon tissue.ConclusionsOur data suggest that GLT could be considered as an alternative dietary approach for the prevention of colitis-associated cancer.
“…As previously demonstrated, polysaccharides isolated from G. lucidum , induced total P450 levels in rat liver, whereas suppressed the activity of CYP1A2, CYP3A and CYP2E1 in hepatic microsomes [41]. Our results indicate that GLT is able to induce XRE/AhR and PXR which regulate expression of CYP1A2 and CYP3A, respectively.…”
BackgroundEpidemiological studies suggest that mushroom intake is inversely correlated with gastric, gastrointestinal and breast cancers. We have recently demonstrated anticancer and anti-inflammatory activity of triterpene extract isolated from mushroom Ganoderma lucidum (GLT). The aim of the present study was to evaluate whether GLT prevents colitis-associated carcinogenesis in mice.Methods/Principal FindingsColon carcinogenesis was induced by the food-borne carcinogen (2-Amino-1-methyl-6-phenylimidazol[4,5-b]pyridine [PhIP]) and inflammation (dextran sodium sulfate [DSS]) in mice. Mice were treated with 0, 100, 300 and 500 mg GLT/kg of body weight 3 times per week for 4 months. Cell proliferation, expression of cyclin D1 and COX-2 and macrophage infiltration was assessed by immunohistochemistry. The effect of GLT on XRE/AhR, PXR and rPXR was evaluated by the reporter gene assays. Expression of metabolizing enzymes CYP1A2, CYP3A1 and CYP3A4 in colon tissue was determined by immunohistochemistry. GLT treatment significantly suppressed focal hyperplasia, aberrant crypt foci (ACF) formation and tumor formation in mice exposed to PhIP/DSS. The anti-proliferative effects of GLT were further confirmed by the decreased staining with Ki-67 in colon tissues. PhIP/DSS-induced colon inflammation was demonstrated by the significant shortening of the large intestine and macrophage infiltrations, whereas GLT treatment prevented the shortening of colon lengths, and reduced infiltration of macrophages in colon tissue. GLT treatment also significantly down-regulated PhIP/DSS-dependent expression of cyclin D1, COX-2, CYP1A2 and CYP3A4 in colon tissue.ConclusionsOur data suggest that GLT could be considered as an alternative dietary approach for the prevention of colitis-associated cancer.
“…Sporocarps were cut into small pieces, dried at 40–50 °C for 48 h and powdered. Gl-PS were extracted by method of Wang et al with slight modification [36]. Briefly, Gl-PS was extracted by hot water from the ganoderma lucidum fruiting body, followed by ethanol precipitation, dialysis, and protein depletion using the Sevag method.…”
The current study evaluated the glucose-lowering effect of ganoderma lucidum polysaccharides (Gl-PS) in streptozotocin (STZ)-induced diabetic mice. The diabetic mice were randomly divided into four groups (8 mice per group): diabetic control group, low-dose Gl-PS treated group (50 mg/kg, Gl-PS), high-dose Gl-PS treated group (150 mg/kg, Gl-PS) and positive drug control treated group (glibenclamide, 4 mg/kg), with normal mice used as the control group. Body weights, fasting blood glucose (FBG), serum insulin and blood lipid levels of mice were measured. After 28 days of treatment with Gl-PS, body weights and serum insulin levels of the Gl-PS treated groups was significantly higher than that of the diabetic control group, whereas FBG levels was significantly lower. Moreover, total cholesterol (TC), triglyceride (TG) and low density lipoprotein cholesterol (LDL-C) levels of the Gl-PS treated groups had dropped, whereas the high density lipoprotein cholesterol (HDL-C) levels had increased. In addition, according to acute toxicity studies, Gl-PS did not cause behavioral changes and any death of mice. These data suggest that Gl-PS has an antihyperglycemic effect. Furthermore, considering the Gl-PS effects on lipid profile, it may be a potential hypolipidaemic agent, which will be a great advantage in treating diabetic conditions associated with atherosclerosis or hyperlipidemia.
“…(Lingzhi), one of the most popular medicinal fungi with a long history in oriental countries, has been extensively used in the treatment of a variety of diseases including cancer, hyperlipidemia, diabetes, neurasthenia, insomnia, hypertension and chronic hepatopathy [10,11]. Ganoderma lucidum polysaccharide (Gl-PS), a glycopeptide isolated from the water-soluble polysaccharides of Ganoderma lucidum, is the primary effective component of Ganoderma lucidum [12][13][14]. Our and some others' previous studies have demonstrated that Gl-PS administration significantly prevented the progression of diabetic renal complications and attenuated myocardial collagen cross-linking and AGEs in diabetic rats, by exerting greater antioxidative activity [15,16].…”
Background/Aims. Refractory wounds in diabetic patients constitute a serious complication that often leads to amputation with limited treatment regimens. The present study was designed to determine the protective effect of Ganoderma lucidum polysaccharide (Gl-PS) on diabetic wound healing and investigate underlying mechanisms. Methods. Streptozotocin (STZ)-induced type 1 diabetic mice with full-thickness excisional wounds were intragastrically administered with 10, 50 or 250 mg/kg/day of Gl-PS. Results. Gl-PS dose-dependently rescued the delay of wound closure in diabetic mice. 50 and 250 mg/kg/day of Gl-PS treatment significantly increased the mean perfusion rate around the wound in diabetic mice. Diabetic conditions markly increased mitochondrial superoxide anion (O2·-) production, nitrotyrosine formation, and inducible nitric oxide synthase (iNOS) activity in wound tissues, which were normalized with Gl-PS treatment. In diabetic wound tissues, the protein level of manganese superoxide dismutase (MnSOD) was unchanged whereas MnSOD activity was inhibited and its nitration was potentiated; Gl-PS administration suppressed MnSOD nitration and increased MnSOD and glutathione peroxidase (GPx) activities. Moreover, Gl-PS attenuated the redox enzyme p66Shc expression and phosphorylation dose-dependently in diabetic mice skin. Conclusion. Gl-PS rescued the delayed wound healing and improved wound angiogenesis in STZ-induced type 1 diabetic mice, at least in part, by suppression of cutaneous MnSOD nitration, p66Shc and mitochondrial oxidative stress.
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