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Effects of cultured Cordyceps mycelia polysaccharide A on tumor neurosis factor-α induced hepatocyte injury with mitochondrial abnormality
- Tang, Huiling, Wei, Weikun, Wang, Wang, Zha, Zhengqi, Li, Ting, Zhang, Zhijie, Luo, Chen, Yin, Hongping, Huang, Fengjie, Wang, Ying
- Carbohydrate polymers 2017 v.163 pp. 43-53
- Cordyceps, Ophiocordyceps sinensis, apoptosis, caspase-3, caspase-9, chromatography, ion exchange, membrane potential, mitochondria, molecular weight, mycelium, peroxisome proliferator-activated receptors, polysaccharides, protective effect, tumor necrosis factor-alpha
- Cordyceps sinensis mycelia polysaccharide A (CPS-A), was isolated from cultured Cordyceps mycelia by 65% alcohol extraction and ion-exchange column chromatography. The molecular weight of CPS-A was 1.2×104Da and the backbone was mainly composed of (1→2)-linked β-d-mannopyranose, (1→2,4)-linked β-d-mannopyranose and (1→4)-linked α-d-glucopyranose with terminal β-d-mannopyranose and α-d-glucopyranose residues. CPS-A played a protective role against TNF-α induced mitochondria injury in L02 cells via up-regulation of mitofusin 2, peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and membrane potential. CPS-A also played a protective role against TNF-α induced L02 cells apoptosis via up-regulation of Bcl-2 and down-regulation of Bid, Bax, cleaved caspase-3, cleaved caspase-9 and ROS production. Moreover, CPS-A attenuated both the normal expression and overexpression of TNF-α receptor 1 (TNFR1) induced by TNF-α administration. In conclusion, CPS-A was involved in TNF-α induced mitochondria abnormality via TNFR1/ROS/Mfn2 pathway.