CYBERMED LIFE - ORGANIC  & NATURAL LIVING

Coriolus versicolor

  • Coriolus versicolor alleviates diabetic cardiomyopathy by inhibiting cardiac fibrosis and NLRP3 inflammasome activation.

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    Abstract Title:

    Coriolus versicolor alleviates diabetic cardiomyopathy by inhibiting cardiac fibrosis and NLRP3 inflammasome activation.

    Abstract Source:

    Phytother Res. 2019 Oct ;33(10):2737-2748. Epub 2019 Jul 23. PMID: 31338905

    Abstract Author(s):

    Yueqiu Wang, Hui Li, Yang Li, Yihan Zhao, Fangfei Xiong, Yining Liu, Hongru Xue, Zhenyu Yang, Sha Ni, Abbas Sahil, Hui Che, Lihong Wang

    Article Affiliation:

    Yueqiu Wang

    Abstract:

    Coriolus versicolor (CV) is a traditional medicine and food mushroom. Our previous study demonstrated that CV extract exhibited anti-hyperglycemia and anti-insulin resistance effects. However, the effect of CV on cardiac function in diabetic cardiomyopathy (DCM) remains unclear. Therefore, we aimed to investigate the effect of CV on cardiac function in diabetes mellitus (DM) rats. We found that the cardiac dysfunction of DM rats was markedly improved by CV extract treatment. CV extract administration significantly attenuated cardiac fibrosis in DM rats, which was accompanied by suppressed transforming growth factor beta 1 (TGF-β1)/Smad signaling as indicated by decreased levels of TGF-β1, p-Smad2, and p-Smad3 and increased Smad7 expression. Moreover, CV extract treatment significantly alleviated cardiac inflammation as shown by decreased levels of NLRP3 receptor, cleaved caspase-1, IL-1β, and IL-18 in DM rats at leastpartly due to the inhibition of the NF-κB. In addition, high-glucose treatment induced cardiac fibrosis and increased cardiac inflammation in cardiac fibroblast cells, but these effects were ameliorated by CV extract treatment. Therefore, we conclude that the protective effect of CV on DCM is associated with the suppression of TGF-β1/Smad signaling and attenuation of NLRP3 inflammasome activation, suggesting that CV extract may be a potential therapeutic agent for DCM.

  • Effect ofMycelia Extract on Exercise Performance and Physical Fatigue in Mice. 📎

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    Abstract Title:

    Effect ofMycelia Extract on Exercise Performance and Physical Fatigue in Mice.

    Abstract Source:

    Int J Med Sci. 2017 ;14(11):1110-1117. Epub 2017 Sep 4. PMID: 29104465

    Abstract Author(s):

    Chun-Sheng Ho, Yu-Tang Tung, Woon-Man Kung, Wen-Ching Huang, Wing-Ki Leung, Chi-Chang Huang, Jyh-Horng Wu

    Article Affiliation:

    Chun-Sheng Ho

    Abstract:

    In this study,mycelia (CVM) was evaluated the ergogenic and anti-fatigue activities. Male ICR mice were divided into four groups (= 8/group) to receive vehicle or CVM by oral gavage for 4 weeks at 0, 615, 1230 or 3075 mg/kg/day, which were respectively designated the vehicle, CVM-1X, CVM-2X and CVM-5X groups. Forelimb grip strength, endurance swimming time, and levels of physical fatigue-associated parameters serum lactate, ammonia, glucose and creatine kinase (CK) after physical challenge were performed to evaluate exercise performance and anti-fatigue activity. Results revealed that the forelimb grip strength of mice in group CVM-1X, CVM-2X and CVM-5X were significantly increased by 1.20-, 1.18- and 1.23-fold, respectively, compared to the vehicle group. After the 15 minute swimming exercise, the levels of serum lactate of CVM-1X, CVM-2X and CVM-5X groups were significantly lower than the vehicle control group by 29%, 23% and 31%, respectively. The levels of ammonia in CVM-1X, CVM-2X and CVM-5X groups were significantly lowered by 22%, 25% and 41%, respectively, compared to the vehicle control group. In addition, the levels of serum CK in CVM-2X and CVM-5X groups were significantly lowered by 13% and 11%, respectively, compared to the vehicle control group. Accordingly, the supplementation with CVM has beneficial effects on performance improvement and anti-fatigue activity, and thus has great potential as a source for natural health products.

  • Induction of S phase cell arrest and caspase activation by polysaccharide peptide isolated from Coriolus versicolor enhanced the cell cycle dependent activity and apoptotic cell death of doxorubicin and etoposide, but not cytarabine in HL-60 cells.

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    Abstract Title:

    Induction of S phase cell arrest and caspase activation by polysaccharide peptide isolated from Coriolus versicolor enhanced the cell cycle dependent activity and apoptotic cell death of doxorubicin and etoposide, but not cytarabine in HL-60 cells.

    Abstract Source:

    Oncol Rep. 2005 Jul;14(1):145-55. PMID: 15944782

    Abstract Author(s):

    Kenrie Pui-Yan Hui, Wai-Hung Sit, Jennifer Man-Fan Wan

    Article Affiliation:

    Department of Zoology, The University of Hong Kong, Pokfulam Road, Hong Kong, SAR, P.R. China.

    Abstract:

    Activation of the cell death program (apoptosis) is a strategy for the treatment of human cancer, and unfortunately a large number of drugs identified as cell cycle-specific agents for killing cancer cells are also toxic to normal cells. The present study demonstrates that the polysaccharide peptide (PSP) extracted from the Chinese medicinal mushroom, Coriolus versicolor, used in combination therapy in China, has the ability to lower the cytotoxicity of certain anti-leukemic drugs via their interaction with cell cycle-dependent and apoptotic pathways. Flow cytometry analysis demonstrated that pre-treatment of PSP (25-100 microg/ml) dose-dependently enhanced the cell cycle perturbation and apoptotic activity of doxorubicin (Doxo) and etoposide (VP-16), but not cytarabine (Ara-C) in human promyelocytic leukemia HL-60 cells. The antagonistic result from combined treatment with Ara-C and PSP may be caused by the removal of HL-60 cells in the G1-S boundary by PSP before exposure to Ara-C. A negative correlation between the increase in apoptotic cell population (pre-G1 peak) with the S-phase cell population expression (R2=0.998), the expression of cyclin E expression (R2=0.872) and caspase 3 activity (R2=0.997) suggests that PSP enhanced the apoptotic machinery of Doxo and VP-16 in a cell cycle-dependent manner and is mediated, at least in part, by the PSP-mediated modulation of the regulatory checkpoint cyclin E and caspase 3. This study is the first to describe the cell cycle mechanistic action of PSP and its interaction with other anticancer agents. Our data support the potential development of PSP as an adjuvant for leukemia treatment, but also imply the importance of understanding its interaction with individual anticancer agents.