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Objective To observe effects of warming acupuncture therapy on expressions of IL-6 and SOCS3 in spinal cord in rats with neuropathic pain; To discuss its mechanism for treating neuropathic pain. Methods Experimental rats were randomly divided into: normal group, model group, warming acupuncture and IL-6 group, with 6 rats in each group. Sciatic nerve chronic constriction injury neuralgia model was established in the model group, without intervention. After modeling for 5 days in the warming acupuncture group, "Pishu" and "Shenshu" acupoints were chosen for warming acupuncture therapy for 10 times. After modeling for 5 days in the IL-6 group, IL-6 group was successfully intrathecally injected 3 times with recombinant IL-6. After finishing all experiments, the mechanical pain behavior was measured with electronic Frye fibers. The mRNA levels of IL-6 and SOCS3 and protein concentration of spinal Iba-1were detected with ELISA and RT-PCR analysis. Results Compared with model group, mechanical withdrawal thresholdsin the warm acupuncture group significantly increased, and the content of Iba-1 decreased significantly (P<0.01); The mRNA level of IL-6 decreased significantly (P<0.01), and the mRNA level of SOCS3 significantly increased (P<0.01). Conclusion Warming acupuncture therapy can reduce the pain response in rats with neuropathic pain through inhibiting spinal cord microglial activation, down-regulating the gene expression of lL-6 and up-regulating the gene expression of SOCS3.
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Objective To observe Effect of baicalin on BV2 cell activation damage caused by rotenone.Methods Rotenone infected BV2 cell viability were detected by MTT assay, and OX42 expression by ICC method assay, the inner cell Ca2 + content by fluorescence spectrophotometry, intracellular iron content by ICP-AES when low concentrations iron of load without damage in cells and extracellular H2 O2 and intracellular content of MDA, NO, NOS with related kits.ResuIts Rotenone exposure BV2 cell reduced cell viability, the expression of cell marker protein OX42 and intracellular Ca2 +content and intracellular iron content were all significantly increased(P<0.05), resulting in oxidative damage to cells.Baicalin reduced OX42 expression of rotenone exposure BV2 cell, increased cells survival, reduced intracellular iron content and H2 O2 release and oxidative damage of BV2(P<0.05).ConcIusion Baicalin inhibits BV2 activation and damage by rotenone-induced, and it has neuroprotective effects.The protection mechanism may relate to reduce iron into cells .