Effects and Mechanism of Kanggu Zengsheng Jiaonang on Osteoarthritis in Rats

Zhou Jun; LIU Xiao-hai; SONG Ya-ling; LV Yao-zhong; WANG Zhen-zhong; XIAO Wei

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Effects and Mechanism of Kanggu Zengsheng Jiaonang on Osteoarthritis in Rats

更新时间：2024-01-04

- Effects and Mechanism of Kanggu Zengsheng Jiaonang on Osteoarthritis in Rats
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 18, Issue 19, Pages: 145-148(2012)
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- Published：2012
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Zhou Jun, LIU Xiao-hai, SONG Ya-ling, et al. Effects and Mechanism of Kanggu Zengsheng Jiaonang on Osteoarthritis in Rats[J]. Chinese journal of experimental traditional medical formulae, 2012, 18(19): 145-148.
DOI：

Zhou Jun, LIU Xiao-hai, SONG Ya-ling, et al. Effects and Mechanism of Kanggu Zengsheng Jiaonang on Osteoarthritis in Rats[J]. Chinese journal of experimental traditional medical formulae, 2012, 18(19): 145-148. DOI：

摘要

目的:探讨抗骨增生胶囊(KGZSJN)对实验性大鼠骨关节炎(OA)的影响。方法:大鼠膝关节腔注射4%木瓜蛋白酶建立OA模型

50只大鼠分为5组

即正常组

模型组

KGZSJN3个剂量ig给予(0.24

0.48

0.96g·kg-1)。末次注射木瓜蛋白酶1周后

开始给药。6周后处死动物

切取膝关节

进行组织学观察

并检测关节滑膜超氧化物歧化酶(SOD)

丙二醛(MDA)活性以及血清一氧化氮(NO)

一氧化氮合酶(NOS)

白介素-1β(IL-1β)

肿瘤坏死因子-α(TNF-α)的水平。结果:KGZSJN可以明显改善OA的膝关节病变;KGZSJN提高关节滑膜SOD的活性

降低关节滑膜MDA水平;KGZSJN降低血清NO

NOS

IL-1β

TNF-α的水平。结论:KGZSJN能有效防治大鼠实验性OA

其效应在一定范围内呈剂量依赖性

其机制可能为提高关节滑膜SOD的活性

降低关节滑膜MDA

抑制血清NO

NOS

IL-1β

TNF-α水平。

Abstract

Objective:To explore the effects of Kanggu Zengsheng Jiaonang(KGZSJN) on experimental osteoarthritis in rats. Method:Animal models of osteoarthritis were obtained in rats by intra-articular injection of 4% papain for three times. Fifty rats were divided into five groups as normal group

model group

and three KGZSJN treatment groups. The animals began receiving drug orally every day one week after the last injection of papain. Six weeks later

all the animals were sacrificed for analysis. Histological examinations were performed on the articular cartilage. In the same time

the activities of superoxide dismutase(SOD)and malondialdehyde(MDA)in synovium were measured

the leves of nitric oxide(NO)

nitric oxide synthase(NOS)

interleukin-1β(IL-1β)

tumor necrosis factor-α(TNF-α)in serum were measured respectively. Result:KGZSJN could significantly reverse cartilage degeneration

and enhanced the activitiy of SOD in synovium

KGZSJN reduced the activity of MDA in synovium

and the levels of NO

NOS

IL-1β

TNF-α in serum. Conclusion:KGZSJN can provide some protection in a dose-dependent manner in this model. The mechanisms are related to the reduction of expression of MDA

NOS

IL-1β

TNF-α

and enhance the activities of SOD.

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