Chronic Treatment with a Water-Soluble Extract from the Culture Medium of Ganoderma lucidum Mycelia Prevents Apoptosis and Necroptosis in Hypoxia/Ischemia-Induced Injury of Type 2 Diabetic Mouse Brain

Type 2 diabetes mellitus has been known to increase systemic oxidative stress by chronic hyperglycemia and visceral obesity and aggravate cerebral ischemic injury. On the basis of our previous study regarding a water-soluble extract from the culture medium of Ganoderma lucidum mycelia (designed as M...

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Published in:Evidence-based complementary and alternative medicine 2015-01, Vol.2015 (2015), p.1-16
Main Authors: Hibino, Yasuhide, Iizuka, Hiroshi, Sakamoto, Takeshi, Matsuzaki, Hirokazu, Kamiuchi, Shinya, Asano, Satoshi, Iwata, Naohiro, Okazaki, Mari, Xuan, Meiyan, Miyano, Yoshiyuki
Format: Article
Language:English
Subjects:
Adipose tissues
Antioxidants
Apoptosis
Chinese medicine
Cytokines
Diabetes
Free radicals
Fungi
Gangrene
Ganoderma lucidum
Gene expression
Hyperglycemia
Hypoxia
Insulin resistance
Ischemia
Kinases
Laboratories
Metabolic disorders
Obesity
Oxidative stress
Pharmaceutical sciences
Pharmaceuticals
Proteins
Rodents
Studies
Tumor necrosis factor-TNF
Type 2 diabetes
Water
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Summary:Type 2 diabetes mellitus has been known to increase systemic oxidative stress by chronic hyperglycemia and visceral obesity and aggravate cerebral ischemic injury. On the basis of our previous study regarding a water-soluble extract from the culture medium of Ganoderma lucidum mycelia (designed as MAK), which exerts antioxidative and neuroprotective effects, the present study was conducted to evaluate the preventive effects of MAK on apoptosis and necroptosis (a programmed necrosis) induced by hypoxia/ischemia (H/I) in type 2 diabetic KKAy mice. H/I was induced by a combination of unilateral common carotid artery ligation with hypoxia (8% O2 for 20 min) and subsequent reoxygenation. Pretreatment with MAK (1 g/kg, p.o.) for a week significantly reduced H/I-induced neurological deficits and brain infarction volume assessed at 24 h of reoxygenation. Histochemical analysis showed that MAK significantly suppressed superoxide production, neuronal cell death, and vacuolation in the ischemic penumbra, which was accompanied by a decrease in the numbers of TUNEL- or cleaved caspase-3-positive cells. Furthermore, MAK decreased the expression of receptor-interacting protein kinase 3 mRNA and protein, a key molecule for necroptosis. These results suggest that MAK confers resistance to apoptotic and necroptotic cell death and relieves H/I-induced cerebral ischemic injury in type 2 diabetic mice.
ISSN:1741-427X
1741-4288
DOI:10.1155/2015/865986