目的：观察痹痛合剂对骨性关节炎(OA)关节软骨细胞形态学变化的影响并探讨其可能的作用机制。方法：将SD雄性大鼠64只随机分为假手术组(A组)、模型组(B组)、硫酸氨基葡萄糖组(C组)和痹痛合剂组(D组)，A组行假手术，B、C、D组采用Hulth法复制OA模型，A组常规饲养，其余各组术后分别加服生理盐水，硫酸氨基葡萄糖溶液和痹痛合剂。术后第8周处死，分别大体观察、光镜400×和电镜下观察关节软骨细胞形态学变化，原位杂交法检测关节软骨细胞中Bc1-2 mRNA表达。结果：B组关节软骨呈典型OA形态学改变，关节软骨细胞中Bc1-2 mRNA表达减弱；C、D组关节软骨轻度退变，形态学方面与A组接近，关节软骨细胞中Bc1-2 mRNA表达显著增强，与B组比较差异有统计学意义(P＜0.01)。结论：痹痛合剂与硫酸氨基葡萄糖能延缓OA大鼠关节软骨的退变，其可能的作用机制是通过提高关节软骨细胞中Bc1-2基因的表达，抑制关节软骨细胞的凋亡。%Objective: To observe the influence ofBiTongmixture on articular cartilage morphology of os-teoarthritis(OA) rats, and explore its possible mechanism. Methods: Sixty-four SD male rats were randomized into sham operation group(A), the model group (B), glucosamine sulfate group (C) andBiTongmixture group (D), the rats in group A were performed with sham operation, the rats in the group B, C and D were replicated by Hulth method, the rats in the group A accepted conventional feeding, the rats in other groups took physiological saline, glu-cosamine sulfate solution andBiTongmixture after the operation respectively. The rats were sacrificed at the eighth week after the operation, cellular morphology of articular cartilage was inspected by gross observation, under light microscope and electron microscope, and the expressions of Bcl-2 mRNA in articular cartilage cells were detected by in situ hybridization(ISH). Results: Articular cartilage showed typical OA morphological changes in the group B, the expressions of Bcl-2 mRNA in articular cartilage cells reduced obviously; articular cartilage degenerated slightly in the groups C and D, morphological changes were similar to the rats in the group A, the expressions of Bcl-2 mR-NA in articular cartilage cells enhanced significantly, it had significant difference compared with the group B(P<0.01). Conclusion:BiTongmixture and glucosamine sulfate solution could delay articular cartilage degeneration of OA rats, and the mechanism might be inhibiting articular cartilage cellular apoptosis by raising the expressions of Bcl-2 mR-NA in articular cartilage cells.
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