Protective Effects of a Water-Soluble Extract from Culture Medium of Lentinus Edodes Mycelia against Neuronal Damage after Hypoxia-Ischemia in Mice
10.1625/jcam.8.99
- VernacularTitle:マウス低酸素脳虚血障害に対する椎茸菌糸体培養培地抽出物の保護作用
- Author:
Meiyan XUAN
;
Mari OKAZAKI
;
Naohiro IWATA
;
Shinya KAMIUCHI
;
Fumiko SUZUKI
;
Hiroshi IIZUKA
;
Yasuhide HIBINO
- Publication Type:Journal Article
- Keywords:
Neuroprotection;
Water-soluble extract of Lentinus edodes mycelia (LEM);
Hypoxia-ischemia;
Oxidative-stress;
Apoptosis
- From:Japanese Journal of Complementary and Alternative Medicine
2011;8(2):99-107
- CountryJapan
- Language:Japanese
-
Abstract:
Objective: Lentinus edodes (Shiitake) is a very popular mushroom in Asian cuisine. The water-soluble extract from culture medium of Lentinus edodes mycelia (LEM), which is commercially available as a nutritional supplement, is prepared by hot-water treatment from a solid medium composed of bagasse and defatted-rice bran overgrown for about 4 months with its mycelia. LEM was previously reported to have antioxidant activity and to suppress various oxidative damages. In this study, the neuroprotective effects of 2-week intake of LEM on cerebral ischemic damage induced by hypoxia/ischemia (H/I) followed by reoxygenation in mice were examined.
Method: Male C57BL/6J mice were divided into three groups, fed for two weeks with the control laboratory powder chow, 0.5% LEM-contained chow, or 1% LEM-contained chow, respectively. Cerebral ischemic damage was induced in the mice by H/I (i.e., unilateral ligation of the carotid artery and exposure of 8%O2 for 30 min). Twenty-four hours after H/I, total plasma oxidative stress, neurological deficits, cerebral infarction volume were evaluated in each group. Furthermore, the number of apoptotic cells in ischemic penumbra, the hippocampal CA1 and CA2, and the somatosensory area of the cortex, were analyzed by TUNEL staining and cleaved caspase-3 immunostaining.
Results: The infarct area assessed 24-h after H/I was extended to the corpus striatum and cortex in the control mice. Treatment of LEM dose dependently improved plasma oxidative stress, neurological deficits, and cerebral infarction volume. Moreover, LEM decreased the levels of dihydroethidium activity as an index of super oxide production and the number of apoptotic cells in ischemic penumbra.
Conclusion: These results show that chronic intake of LEM relieves the hypoxia-induced cerebral ischemic injury, which may be attributed to the antioxidant effects of LEM.
