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目的:探讨芍药苷(Pae)对脂多糖(LPS)诱导的小鼠急性炎性脑损伤的保护作用。方法:将雄性Balb/c小鼠随机分为正常对照组、模型组及芍药苷低、高剂量组,腹腔注射给药,1次/d,连续7 d。7 d后除正常对照组外,其余各组均腹腔注射LPS造模,6 h后取材。ELISA法检测血清TNF-α、IL-1β含量;比色法检测脑组织中髓过氧化物酶(MPO)、一氧化氮(NO)及诱导型一氧化氮合酶(i NOS)水平;RT-PCR法检测脑组织中TNF-α、IL-1β及i NOS的mRNA表达;Western blot法检测脑组织中IκB-α、NF-κB、P-IκB-α蛋白表达水平。结果:芍药苷可降低内毒素致急性脑损伤小鼠血清TNF-α和IL-1β含量,降低脑组织中MPO、i NOS活性及NO含量;降低脑组织中TNF-α、IL-1β和i NOS mRNA表达;可使脑组织中IκB磷酸化蛋白表达减少。结论:芍药苷能减轻LPS诱导的小鼠急性炎症脑损伤,其机制可能与抑制NF-κB的核转位,从而抑制炎症因子的表达有关。
Objective: To investigate the protective effect of paeoniflorin on lipopolysaccharide (LPS) -induced acute inflammatory brain injury in mice. Methods: Male Balb / c mice were randomly divided into normal control group, model group and paeoniflorin low and high dose group, intraperitoneal injection once a day for 7 days. After 7 days, except the normal control group, the other groups were given intraperitoneal injection of LPS, and the materials were obtained 6 h later. The contents of TNF-α and IL-1β in serum were detected by ELISA. The levels of MPO, NO and iNOS were determined by colorimetry. The mRNA expressions of TNF-α, IL-1β and iNOS in brain tissue were detected by PCR. The expression of IκB-α, NF-κB and P-IκB-α in brain tissue were detected by Western blot. Results: Paeoniflorin could decrease the levels of TNF-α and IL-1β in serum in acute brain injury induced by endotoxin, reduce the activity of MPO, i NOS and the content of NO in brain, decrease the contents of TNF-α, IL- NOS mRNA expression; brain IκB phosphorylation protein expression can be reduced. CONCLUSION: Paeoniflorin can relieve the acute inflammatory brain injury induced by LPS in mice. The mechanism may be related to the inhibition of the nuclear translocation of NF-κB and the inhibition of the expression of inflammatory cytokines.