现代中西医结合杂志
現代中西醫結閤雜誌
현대중서의결합잡지
MODERN JOURNAL OF INTEGRATED TRADITIONAL CHINESE AND WESTERN MEDICINE
2014年
28期
3093-3095
,共3页
陈守中%郑云生%王志文%王国权
陳守中%鄭雲生%王誌文%王國權
진수중%정운생%왕지문%왕국권
抗骨增生片%骨关节炎%软骨组织%胰岛素样生长因子1%p38 丝裂原活化蛋白激酶
抗骨增生片%骨關節炎%軟骨組織%胰島素樣生長因子1%p38 絲裂原活化蛋白激酶
항골증생편%골관절염%연골조직%이도소양생장인자1%p38 사렬원활화단백격매
Kangguzengsheng tablet%osteoarthritis%cartilage%IGF-1%p38MAPK
目的：观察抗骨增生片对兔膝骨关节炎软骨组织病理形态及胰岛素样生长因子1（IGF-1）、p38丝裂原活化蛋白激酶（p38MAPK）表达的影响。方法将40只成年雄性大耳白兔随机分为正常组（A组）10只和造模组30只。膝关节腔内注射1.6%木瓜蛋白酶，造成兔膝骨关节炎模型。造模成功后，再将造模组随机分为模型组（B 组）、抗骨增生片低剂量组（C组）、高剂量组（D组）各10只，C、D组分别灌胃0.36，0.72 g/（kg·d）的抗骨增生片，1次/d；A、B组每天灌胃等量生理盐水。4周后，取膝关节软骨组织，观察软骨组织病理形态变化，用免疫组化法检测软骨组织中 IGF -1、p38MAPK 的表达情况。结果 C 组、D 组软骨组织破坏程度较 B组明显减轻（P 均﹤0.01）；C 组、D 组 IGF -1的表达较 B 组显著升高（P均﹤0.05），p38MAPK的表达较 B组显著降低（P均﹤0.01）。结论抗骨增生片能抑制兔骨关节炎软骨病理损害，机制可能与其上调 IGF-1、下调 p38MAPK的表达，抑制过度的软骨细胞凋亡有关。
目的：觀察抗骨增生片對兔膝骨關節炎軟骨組織病理形態及胰島素樣生長因子1（IGF-1）、p38絲裂原活化蛋白激酶（p38MAPK）錶達的影響。方法將40隻成年雄性大耳白兔隨機分為正常組（A組）10隻和造模組30隻。膝關節腔內註射1.6%木瓜蛋白酶，造成兔膝骨關節炎模型。造模成功後，再將造模組隨機分為模型組（B 組）、抗骨增生片低劑量組（C組）、高劑量組（D組）各10隻，C、D組分彆灌胃0.36，0.72 g/（kg·d）的抗骨增生片，1次/d；A、B組每天灌胃等量生理鹽水。4週後，取膝關節軟骨組織，觀察軟骨組織病理形態變化，用免疫組化法檢測軟骨組織中 IGF -1、p38MAPK 的錶達情況。結果 C 組、D 組軟骨組織破壞程度較 B組明顯減輕（P 均﹤0.01）；C 組、D 組 IGF -1的錶達較 B 組顯著升高（P均﹤0.05），p38MAPK的錶達較 B組顯著降低（P均﹤0.01）。結論抗骨增生片能抑製兔骨關節炎軟骨病理損害，機製可能與其上調 IGF-1、下調 p38MAPK的錶達，抑製過度的軟骨細胞凋亡有關。
목적：관찰항골증생편대토슬골관절염연골조직병리형태급이도소양생장인자1（IGF-1）、p38사렬원활화단백격매（p38MAPK）표체적영향。방법장40지성년웅성대이백토수궤분위정상조（A조）10지화조모조30지。슬관절강내주사1.6%목과단백매，조성토슬골관절염모형。조모성공후，재장조모조수궤분위모형조（B 조）、항골증생편저제량조（C조）、고제량조（D조）각10지，C、D조분별관위0.36，0.72 g/（kg·d）적항골증생편，1차/d；A、B조매천관위등량생리염수。4주후，취슬관절연골조직，관찰연골조직병리형태변화，용면역조화법검측연골조직중 IGF -1、p38MAPK 적표체정황。결과 C 조、D 조연골조직파배정도교 B조명현감경（P 균﹤0.01）；C 조、D 조 IGF -1적표체교 B 조현저승고（P균﹤0.05），p38MAPK적표체교 B조현저강저（P균﹤0.01）。결론항골증생편능억제토골관절염연골병리손해，궤제가능여기상조 IGF-1、하조 p38MAPK적표체，억제과도적연골세포조망유관。
Objective It is to observe the effect of Kangguzengsheng tablet on pathomorphlogy and expression of IGF -1 and p38 mitogen-activated proteikinase( p38MAPK)in cartilage of the rabbit of knee osteoarthritis( KOA). Methods 40 healthy male rabbits were randomly divided into normal control group(group A,n=10)and model control group(n=30). The KOA rabbit models were induced by injection 1. 6% papain into the cavum articulare. After the models were successfully established,the model control group was randomly divided into model group( group B),low dosage of Kangguzengsheng tablet group( group C)and high dosage group( group D),each group had 10 rabbits. Group C and group D were respectively given Kangguzengsheng tablet 0. 36,0. 72 g/(kg·d)once a day by intragastric administration,and group A and group B was given the same dosage of normal saline. After 4 weeks,cartilage tissue of knee joint was gotten to observe the pathomorphlogy chan-ges,and the expression of IGF -1 and p38MAPK were detected by immunohistochemistry technique. Results The cartilage damage in group group C and group D was obviously relieved compared with that in group B(P ﹤0. 01). The expression of IGF -1 was significantly higher while the expression of p38MAPK was lower in group C and group D than that in group B(P﹤0. 01 or P﹤0. 05). Conclusion Kangguzengsheng tablet can inhibit the pathomorphlogy damage of joint cartilage in rabbits, and its mechanism may be that it can increase the expression of IGF-1 and reduce the expression of p38MAPK,and inhibit excessive cartilage cell apoptosis.
