<p>Effect and Mechanism of <em>Ganoderma lucidum</em> Spores on Alleviation of Diabetic Cardiomyopathy in a Pilot in vivo Study</p>

Abstract

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 was to evaluate the hyperglycemia-mediated cardiomyopathy protection and mechanisms of GLS in streptozotocin (STZ)induced diabetic rats. 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, among them, 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 antioxidants, 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 collagen fibrosis 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 Bcl-2. Moreover, GLS treatment significantly increased the phosphorylation of key proteins involved in PI3K/AKT pathway, eg, 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 stimulation of the PI3K/Akt/mTOR signaling pathway.

Ganoderma lucidum Polysaccharide Peptide Reduces Oxidative Stress and Improves Renal Function in Patient with Cardiometabolic Syndrome

“…These results showed that GLPP-treated subjects had lower oxidative stress suggesting the GLPP could be potential for preventing development of oxygen stress-induced inflammation. The decrease of MDA and significant increase of SOD in the GLPP treatment group were also reported in atherosclerotic (26) and type 2 diabetes mellitus rats studies (27,28). In human, with the treatment of GLPP, subjects with atrial fibrillation (24) and stable angina pectoris (17) showed a decrease of MDA level.…”

Mechanisms and Therapeutic Prospects of Diabetic Cardiomyopathy Through the Inflammatory Response

“…Certain natural compounds can ameliorate cardiac inflammation by directly modulating inflammatory responses. Probiotics, fungi, and medicinal plants exert an anti-inflammatory action via downregulation of TLR4 expression ( Chiang et al, 2021 ) and reduction of IL-1β, TNFα, MCP-1, and TGFβ ( Wang et al, 2018 ; Shaher et al, 2020 ), subsequently preserving cardiac structure and function in T1DM rodents. Moreover, hederagenin, a plant extract, improves cardiac function by diminishing secretion of pro-inflammatory cytokines and decreasing NF-κB transcriptional activity in db/db mice ( Li Y. et al, 2019 ).…”

Effects and Mechanism of Ganoderma lucidum Polysaccharides in the Treatment of Diabetic Nephropathy in Streptozotocin-Induced Diabetic Rats

“…Several extracts of Ganoderma lucidum showed amelioration in this progress in a review [ 50 ], e.g., one study [ 51 ] showed that proteoglycan isolated from Ganoderma lucidum fruiting bodies shows protection renal morphology in diabetic mice in a dose-dependently (75, 250, and 450 mg/kg) manner during a 8-week treatment. According to previous research, the mechanism appears also via directly elimination reactive oxygen species, suppresses lipid peroxidation, and indirectly scavenges the radicals via activating antioxidant enzyme systems and chelation with metal ion by forming crossbridge between carboxyl groups decreasing reactive oxygen species generation [ 52 – 60 ]. This study showed that the expressions of the inflammatory factors IL-6, IL-1 β , and TNF- α in the diabetic group were significantly increased, while they were reduced significantly after GLP treatment.…”