BACKGROUND:Current studies have confirmed that Ganoderma lucidum polysaccharides can promote nerve regeneration in neurodegeneration-related diseases.The occurrence of neurodegenerative diseases is closely related to mitochondrial dysfunction,but the role of Ganoderma lucidum polysaccharides on the regulation of apoptosis and mitochondrial function in neurodegenerative diseases is not yet clarified. OBJECTIVE:To explore the regulatory effects and mechanisms of Ganoderma lucidum polysaccharides on apoptosis and mitochondrial dysfunction in H2O2-induced SH-SY5Y cells. METHODS:SH-SY5Y cells were divided into three groups:control group,H2O2 group,and Ganoderma lucidum polysaccharides group.Cells in the control group were normally cultured.Cells in the H2O2 group were treated with 300 μmol/L H2O2 for 24 hours.In the Ganoderma lucidum polysaccharides group,the intervention with 300 μg/L Ganoderma lucidum polysaccharides was conducted first for 1-2 hours,followed by the addition of 300 μmol/L H2O2 for 24 hours.The mitochondrial membrane potential was detected by JC-1 kit.Apoptosis was detected by TUNEL staining kit.The activities of malondialdehyde and superoxide dismutase were detected by malondialdehyde test kit and superoxide dismutase test kit,respectively.The apoptosis and expression of mitochondrial dynamics-related proteins were detected by immunofluorescence staining and western blot assay. RESULTS AND CONCLUSION:(1)Compared with the control group,the mitochondrial membrane potential and superoxide dismutase activity were significantly reduced,as well as apoptotic rate and malondialdehyde levels were significantly increased in the H2O2 group(P<0.05).After treatment with Ganoderma lucidum polysaccharides,the membrane potential and superoxide dismutase activities were significantly increased,and apoptotic rate and malondialdehyde levels were significantly reduced compared with the H2O2 group(P<0.05).(2)The expression levels of pro-apoptotic proteins Bax and Caspase-3 were significantly increased,but the expression of anti-apoptotic protein Bcl-2 was significantly decreased in the H2O2 group compared with the control group(P<0.05).Compared with the H2O2 group,the levels of Bax and Caspase-3 were significantly decreased,but the expression of anti-apoptotic protein Bcl-2 was significantly increased in the Ganoderma lucidum polysaccharides group(P<0.05).(3)Compared with the control group,the expression of mitochondrial splitting proteins Fis1 and p-Drp1 was significantly increased,but the expression of mitochondrial fusion proteins OPA1,Mfn1,and Mfn2 was decreased in the H2O2 group(P<0.05).Compared with the H2O2 group,Fis1 and p-Drp1 expression was significantly reduced,but the expression levels of OPA1,Mfn1,and Mfn2 were significantly increased in the Ganoderma lucidum polysaccharides group(P<0.05).(4)The above results confirm that Ganoderma lucidum polysaccharides can attenuate H2O2-induced oxidative stress damage and apoptosis in SH-SY5Y cells by ameliorating mitochondrial dysfunction.

Objective : To investigate the mechanism of AMD3100 reversing the resistance of human hepatocellular carcinoma cells to Sorafenib by regulating carbonic anhydrase IX ( CA9) and chemokine receptor 4 ( CXCR 4 ) . Methods : The Sorafenib resistant cell lines Huh7 / Sor and HepG2 / Sor were established from human hepatocellular carcinoma cells Huh7 and HepG2．The effects of Sorafenib alone or in combination with AMD3100 on the proliferation of Huh7，HepG2，Huh7 / Sor，HepG2 / Sor cells were detected．The difference of invasive ability between Sorafenib resistant cells and non-resistant cells，and the effect of AMD3100 on the invasive ability of hepatocellular carcinoma cells were observed．And the regulation effect of Sorafenib alone or in combination with AMD3100 on the expression of CA9 and CXCR4 proteins in Huh7，HepG2，Huh7 / Sor and HepG2 / Sor cells was detected. Results: Compared with the Control group，AMD3100 (50 μmol / L) increased the inhibitory effect of Sorafenib on the proliferation of Huh7 / Sor and HepG2 / Sor cells (P＜0．05) ．Compared with Huh7 cells，the invasive ability of Sorafenib resistant Huh7 / Sor cells was significantly enhanced (P＜0. 05) ，and AMD 3100 (50 μmol / L) decreased the invasive ability of Huh7 and Huh7 / Sor cells (P＜0．05) ．Compared with Huh7 and HepG2 cells，the protein expression of CA9 and CXCR4 in Huh7 / Sor and HepG2 / Sor cells increased (P＜0. 05) ．AMD3100 (50 μmol / L) down-regulated the protein expression of CA9 and CXCR4 in Huh7，HepG2，Huh7 / Sor and HepG2 / Sor cells (P ＜0. 05 ) . Conclusion AMD3100 can reduce the resistance of human hepatocellular carcinoma cells to Sorafenib by downregulating the expression of CA9 and CXCR4，and enhance the inhibition of Sorafenib on the proliferation and invasion of human hepatocellular carcinoma cells.

Objective To explore the effect of traditional Chinese massage on upper limbs spasticity in stroke patients who accepted Botulinum toxin type A (BTX-A) injection. Methods 74 stroke patients with upper limbs spasticity were divided into treatment group (n=36)and control group (n=38). The control group received BTX-A injection, and the treatment group received massage after injection. Both groups received rehabilitation training after injection and were assessed with modified Ashworth scale, Fugl-Meyer assessment and modified Barthel index before and 2 weeks, 4 weeks, 8 weeks and 12 weeks after treatment. Results All the scores of assessments improved in both groups after treatment (P<0.001), and there was no significant difference between them (P>0.05). Conclusion Addition of traditional Chinese massage doesn't work more on spasticity of upper limbs after stroke when accepted BTX-A injection.