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Han Z.-H.,Luqiao Hospital of Taizhou Enze Medical Center Group | Ye J.-M.,Luqiao Hospital of Taizhou Enze Medical Center Group | Wang G.-F.,Luqiao Hospital of Taizhou Enze Medical Center Group
International Journal of Biological Macromolecules

Hericium erinaceus polysaccharide (HEP) is a traditional Chinese medicine. In the present study, chemical composition and antioxidant activity of HEP was investigated. HPLC analysis showed that the HEP was composed of xylose (7.8%), ribose (2.7%), glucose (68.4%), arabinose (11.3%), galactose (2.5%) and mannose (5.2%). HEP was pre-administered to mice by gavage at a dose of 300. mg/kg for 15 days. Results found that HEP preadministration resulted in a significant decline in blood urea nitrogen (BUN), serum creatinine (Scr) and increase in creatinine clearance (CrCI) levels in HEP-pretreated group compared to renal ischemia reperfusion (IR) group. Malondialdehyde (MDA) level significantly increased, whereas Level of reduced glutathione (GSH) markedly decreased in renal IR animals. These results indicate that IR induced renal oxidative injury damage, as indicated by a increase in MDA level, and decrease in GSH level as well as the antioxidant enzymes activity. Such effects reflect that HEP can significantly decrease lipid peroxidation level and increase antioxidant enzymes activities in experimental animals. © 2012 Elsevier B.V. Source

Zhou R.-J.,Luqiao Hospital of Taizhou Enze Medical Center Group | Xu X.-Y.,Luqiao Hospital of Taizhou Enze Medical Center Group | Liu B.-X.,Luqiao Hospital of Taizhou Enze Medical Center Group | Dai W.-Z.,Luqiao Hospital of Taizhou Enze Medical Center Group | And 7 more authors.
International Journal of Molecular Medicine

The constitutive activation of signal transducer and activator of transcription 3 (STAT3) contributes to resistance to temozolomide (TMZ) in glioblastoma multiforme (GBM). The aim of this study was to explore the biological role of microRNA-31 (miR-31) in GBM, particularly its role in the regulation of TMZ chemosensitivity. For this purpose, the human GBM cell lines, U251 and U87, were transfected with a miR-31 precursor (pre-miR-31), and cell proliferation, apoptosis and STAT3 phosphorylation were then assessed. To evaluate the effects of miR-31 on TMZ cytotoxicity, the cells were transfected with pre-miR-31 and exposed to 100 μM TMZ for 72 h prior to cell proliferation and apoptosis analysis. A constitutively active STAT3 mutant was co-transfected with pre-miR-31 into the cells to confirm the mediating role of STAT3 signaling. The enforced expression of miR-31 significantly reduced cell proliferation and induced mitochondrial apoptosis, as manifested by the loss of mitochondrial membrane potential and the increase in caspase-9 and caspase-3 activity. The phosphorylation level of STAT3 was significantly decreased by the overexpression of miR-31. The co-delivery of the constitutively active STAT3 mutant blocked the tumor suppressive effects of miR-31. In addition, miR-31 overexpression significantly enhanced the cytotoxic effects of TMZ on the GBM cells, as evidenced by the accelerated suppression of cell proliferation and the induction of apoptosis. The chemosensitizing effects of miR-31 were significantly impaired by the expression of the constitutively active STAT3 mutant. Taken together, our results indicate that miR-31 triggers mitochondrial apoptosis and potentiates TMZ cytotoxicity in GBM cells largely through the suppression of STAT3 activation. Thus, the restoration of miR-31 expression may be of therapeutic beenefit in the treatment of GBM. Source

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