CAJ | 학술논문

目的：观察壮腰通痹汤对大鼠椎间盘退变模型血清基质金属蛋白酶及椎间盘组织形态学的影响，探讨壮腰通痹汤治疗腰椎间盘退变性疾病的作用机理。方法：18只SD大鼠随机分成空白组、模型组及壮腰通痹汤组，采用纤维环穿刺法建立大鼠椎间盘退变模型，壮腰通痹汤灌胃治疗2周后用ELISA法测定各组血清MMP-1、MMP-3、TIMP-1的浓度，椎间盘组织行HE染色。结果：模型组MMP-1及MMP-3浓度均高于空白组（P<0.05），壮腰通痹汤组MMP-1及MMP-3浓度均显著低于模型组（P<0.05），壮腰通痹汤组TIMP-1浓度显著高于空白组及模型组（P<0.05）；HE染色，模型组有明显病理改变，壮腰通痹汤组显示椎间盘组织病理损伤有一定修复。结论：壮腰通痹汤能提高椎间盘组织的自身修复能力，其椎间盘保护作用可能通过调节异常MMP-1、MMP-3、TIMP-1实现。
목적：관찰장요통비탕대대서추간반퇴변모형혈청기질금속단백매급추간반조직형태학적영향，탐토장요통비탕치료요추간반퇴변성질병적작용궤리。방법：18지SD대서수궤분성공백조、모형조급장요통비탕조，채용섬유배천자법건립대서추간반퇴변모형，장요통비탕관위치료2주후용ELISA법측정각조혈청MMP-1、MMP-3、TIMP-1적농도，추간반조직행HE염색。결과：모형조MMP-1급MMP-3농도균고우공백조（P<0.05），장요통비탕조MMP-1급MMP-3농도균현저저우모형조（P<0.05），장요통비탕조TIMP-1농도현저고우공백조급모형조（P<0.05）；HE염색，모형조유명현병리개변，장요통비탕조현시추간반조직병리손상유일정수복。결론：장요통비탕능제고추간반조직적자신수복능력，기추간반보호작용가능통과조절이상MMP-1、MMP-3、TIMP-1실현。
Objective:To observe the effects of Zhuangyao Tongbi decoction on matrix metalloproteinases and histomorphology of lumbar disc degen-eration of rat model, and explore the mechanism of Zhuangyao Tongbi Decoction for degenerative lumbar disc disease. Methods:18 SD rats were randomly divided into blank group, model group and decoction group, establishing rat model of intervertebral disc degeneration with anulus punc-ture, after 2 weeks of gastric gavage of Zhuangyao Tongbi decoction, ELISA method was used to measure the serum concentration of MMP-1, MMP-3 and TIMP-1, intervertebral disc tissue with HE staining. Results:MMP-1 and MMP-3 concentrations of model group were higher than those of blank group (P<0.05), MMP-1 and MMP-3 concentration of decoction group were significantly lower than those of model group (P<0.05), and TIMP-1 concentration of decoction group was significantly higher than that of blank and model group (P<0.05); according to HE staining, model group had obvious pathological changes, decoction group showed that pathological injury of intervertebral disc tissue had certain repair capability. Conclusion:Zhuangyao Tongbi decoction can improve the self-repairing capability of intervertebral disc tissue, the protective effect of intervertebral disc is likely to be achieved according to regulating abnormal MMP-1, MMP-3 amd TIMP-1.