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Associated targets of the antioxidant cardioprotection of Ganoderma lucidum in diabetic cardiomyopathy by using open targets platform: a systematic reviewShaher, Fahmi; Qiu, Hong-Bin; Wang, Shuqiu; Hu, Yu; Wang, Weiqun; Zhang, Yu; Wei, Yao; AL-ward, Hisham; Abdulghani, Mahfoudh A. M.; Alenezi, Sattam Khulaif; et al. (Hindawi, 2020-07-25)Even with substantial advances in cardiovascular therapy, the morbidity and mortality rates of diabetic cardiomyopathy (DCM) continually increase. Hence, a feasible therapeutic approach is urgently needed. Objectives. This work is aimed at systemically reviewing literature and addressing cell targets in DCM through the possible cardioprotection of G. lucidum through its antioxidant effects by using the Open Targets Platform (OTP) website. Methods. The OTP website version of 19.11 was accessed in December 2019 to identify the studies in DCM involving G. lucidum. Results. Among the 157 cell targets associated with DCM, the mammalian target of rapamycin (mTOR) was shared by all evidence, drug, and text mining data with 0.08 score association. mTOR also had the highest score association 0.1 with autophagy in DCM. Among the 1731 studies of indexed PubMed articles on G. lucidum published between 1985 and 2019, 33 addressed the antioxidant effects of G. lucidum and its molecular signal pathways involving oxidative stress and therefore were included in the current work. Conclusion. mTOR is one of the targets by DCM and can be inhibited by the antioxidative properties of G. lucidum directly via scavenging radicals and indirectly via modulating mTOR signal pathways such as Wnt signaling pathway, Erk1/2 signaling, and NF-κB pathways.
Effect and mechanism of Ganoderma lucidum spores on alleviation diabetic cardiomyopathy in a pilot in vivo studyShaher, Fahmi; Wang, Shuqiu; Qiu, Hong-Bin; Hu, Yu; Zhang, Yu; Wang, Weiqun; AL-ward, Hisham; Abdulghani, Mahfoudh A. M.; Baldi, Salem; Zhou, Shaobo; et al. (Dove Press, 2020-12-07)Background: Ganoderma lucidum spores (GLS) exhibit disease prevention properties, but no study has been carried out on the anti-diabetic cardiomyopathy property of GLS. The aim of this study is to evaluate the hyperglycemia-mediated cardiomyopathy protection and mechanisms of GLS in diabetic rats induced by streptozotocin (STZ). Methods: Male SD rats were randomly divided into three groups. Two groups were given STZ (50 mg/kg, i.p.) treatment and when their fasting plasma glucose was above 16.7 mmol/L, one group was given placebo, as diabetic group; and another group was given GLS (300 mg/kg) treatment. The group without STZ treatment was given placebo as a control group. The experiment lasted 70 days. The histology of myocardium and biomarkers of antioxidant, myocardial injury, pro-inflammatory cytokines, pro-apoptotic proteins and phosphorylation of key proteins in PI3K/AKT pathway were assessed. Results: Biochemical analysis showed that GLS treatment significantly reduced the blood glucose (-20.3%) and triglyceride (-20.4%) levels compared to diabetic group without treatment. GLS treatment decreased the content of MDA (-25.6%) and activity of lactate dehydrogenase (-18.9%) but increased the activity of GSH-Px (65.4%). Western blot analysis showed that GLS treatment reduced the expression of both alpha-smooth muscle actin and brain natriuretic peptide. Histological analysis on the cardiac tissue micrographs showed that GLS treatment reduced the collagen fibroses and glycogen reactivity in myocardium. Both western blot and immunohistochemistry analyses showed that GLS treatment decreased the expression levels of pro-inflammatory factors (cytokines IL-1β, and TNF-α) as well as apoptosis regulatory proteins (Bax, caspase-3 and -9), but increased the Bcl-2. Moreover, GLS treatment significantly increased the phosphorylation of key proteins involved in PI3K/AKT pathway, e.g. p-AKT p-PI3K and mTOR. Conclusion: The results indicated that GLS treatment alleviates diabetic cardiomyopathy by reducing hyperglycemia, oxidative stress, inflammation, apoptosis and further attenuating the fibrosis and myocardial dysfunction induced by STZ through the stimulation of the PI3K/Akt/mTOR signaling pathway.