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目的分析六味地黄丸对兔退变椎间盘肿瘤坏死因子-α(TNF-α)与白介素1β(IL-1β)表达的影响。方法选择8月龄成年新西兰兔30只利用异常应力负荷及椎间失稳法建立新西兰兔腰椎椎间盘退变模型,处死4只病理切片确认模型成功后,取6只备用作为模型组,余20只随机分为观察组与对照组各10只,同时取同月龄的正常新西兰兔6只作为正常组。对照组造模成功后,给予正常饮食及日常负重活动。观察组在对照组基础上给予六味地黄丸和治疗。分别与用药前及用药后3周采用酶联免疫吸附法测定椎间盘组织中的TNF-α与IL-1β表达水平。结果造模成功后用药前取模型组新西兰兔椎间盘组织TNF-α及IL-1β水平均高于正常组,差异有统计学意义(P<0.05)。用药后3周观察组TNF-α及IL-1β水平均低于对照组,差异均有统计学意义(P<0.05)。结论六味地黄丸能抑制兔退变椎间盘损伤加重,起到延缓椎间盘损伤的作用,其机制可能与抑制退变椎间盘炎性因子的过度表达有关。
Objective To analyze the effect of Liuweidihuangwan on the expression of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in degenerative intervertebral disc in rabbits. Methods Thirty New Zealand white rabbits (8 months old) were used to establish a New Zealand rabbit model of lumbar disc degeneration by means of abnormal stress load and intervertebral instability method. After the four pathological sections were killed, 6 models were selected as the model group and 20 Randomly divided into observation group and control group of 10, while taking the same age of normal New Zealand rabbits 6 as a normal group. The control group after successful modeling, giving normal diet and daily weight-bearing activities. The observation group was given Liuweidihuang Pills and the treatment on the basis of the control group. The levels of TNF-α and IL-1β in intervertebral disc tissue were determined by enzyme-linked immunosorbent assay before administration and 3 weeks after treatment. Results After modeling, the levels of TNF-α and IL-1β in the intervertebral disc tissue of New Zealand rabbits before model administration were higher than those of the normal group, with statistical significance (P <0.05). The levels of TNF-α and IL-1β in the observation group after 3 weeks of treatment were lower than those in the control group, with statistical significance (P <0.05). Conclusion Liuweidihuang Pills can inhibit the degeneration of intervertebral disc in rabbits and play an important role in delaying the injury of intervertebral disc. The mechanism may be related to the suppression of the excessive expression of degenerative disc inflammatory factors.