scholarly journals Protective Effects of a Water-Soluble Extract from Culture Medium of Lentinus Edodes Mycelia against Neuronal Damage after Hypoxia-Ischemia in Mice

2011 ◽  
Vol 8 (2) ◽  
pp. 99-107
Author(s):  
Meiyan XUAN ◽  
Mari OKAZAKI ◽  
Naohiro IWATA ◽  
Shinya KAMIUCHI ◽  
Fumiko SUZUKI ◽  
...  
Keyword(s):  
Culture Medium ◽  
Neuronal Damage ◽  
Water Soluble ◽  
Protective Effects ◽  
Lentinus Edodes ◽  
Soluble Extract ◽  
Hypoxia Ischemia ◽  
Water Soluble Extract

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

2015 ◽  
Vol 2015 ◽  
pp. 1-16 ◽  
Author(s):  
Meiyan Xuan ◽  
Mari Okazaki ◽  
Naohiro Iwata ◽  
Satoshi Asano ◽  
Shinya Kamiuchi ◽  
...  
Keyword(s):  
Cell Death ◽  
Culture Medium ◽  
Ischemic Injury ◽  
Water Soluble ◽  
Soluble Extract ◽  
Hypoxia Ischemia ◽  
Water Soluble Extract ◽  
Cerebral Ischemic ◽  
Type 2 Diabetic

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 ofGanoderma lucidummycelia (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% O2for 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.

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