虫草素通过调节COX-2/PGE2信号通路促进骨质疏松大鼠的骨折愈合
Cordycepin promotes fracture healing in osteoporosis rats by regulating COX-2/PGE2 signal pathway
  
DOI:10.3969/j.issn.1006-7108.2023.09.016
中文关键词:  虫草素  骨质疏松  COX-2/PGE2信号通路  骨折愈合
英文关键词:cordycepin  osteoporosis  COX-2/PGE2 signal pathway  fracture healing
基金项目:2018年度武汉市医学科研项目(WX18Q26);国家自然科学基金(81802137)
作者单位
胡锐 万兰婷 安颖 朱进 李善庆 严立* 武汉市第四医院手外科湖北 武汉 430033 
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中文摘要:
      目的 探讨虫草素(Cordycepin)调控环氧化酶2(COX-2)/前列腺素E2(PGE2)信号通路对骨质疏松大鼠骨折愈合的影响。方法 制备骨质疏松大鼠模型,将大鼠分为Sham组、Model组、Cordycepin组(10 mg/kg腹腔注射)、Cordycepin+NS-398组(腹腔注射10 mg/kg的Cordycepin+10 mg/kg的COX-2抑制剂),分别检测骨折愈合情况、骨密度(BMD)及生物力学性能,HE染色观察骨痂组织病理学变化,ELISA法检测血清ALP、CTX-Ⅰ、OC水平及骨痂组织COX-2、PGE2、cAMP水平,免疫组化法检测骨痂组织COX-2、VEGF表达。结果 与Sham组比较,Model组骨折线明显,X光片评分、BMD、骨最大负荷与刚度、ALP、OC水平显著降低、骨组织COX-2、PGE2、cAMP、VEGF表达水平显著降低,CTX-Ⅰ水平显著升高(P<0.05);与Model组比较,Cordycepin组X光片评分、BMD、骨最大负荷与刚度、ALP、OC水平显著升高、骨组织COX-2、PGE2、cAMP、VEGF表达水平显著升高,CTX-Ⅰ水平显著降低(P<0.05);NS-398可逆转Cordycepin对骨质疏松大鼠骨折愈合的促进作用。结论 虫草素可能通过激活COX-2/PGE2信号通路,促进骨质疏松大鼠的骨折愈合。
英文摘要:
      Objective To investigate the effects of cordycepin on fracture healing by regulating cyclooxygenase-2 (COX-2) / prostaglandin E2 (PGE2) signal pathway in rats with osteoporosis. Methods Rat osteoporosis model was prepared. The rats were grouped into Sham group, Model group, Cordycepin group (10 mg/kg intraperitoneal injection), and Cordycepin+NS-398 group (10 mg/kg Cordycepin+10 mg/kg COX-2 inhibitor intraperitoneal injection). The fracture healing, bone mineral density (BMD), and biomechanical properties were measured respectively. HE staining was used to observe the histopathological changes of the callus. Serum levels of ALP, CTX-Ⅰ, OC, and the levels of COX-2, PGE2 and cAMP in the callus tissue were detected with ELISA. The expressions of COX-2 and VEGF in the callus were detected with immunohistochemistry. Results Compared with those in Sham group, the fracture line of Model group was obvious, X-ray score, BMD, maximum load, and stiffness of callus, and the levels of ALP and OC reduced obviously, the expression levels of COX-2, PGE2, cAMP and VEGF in bone tissue decreased obviously, and the level of CTX-Ⅰ increased obviously (P<0.05). Compared with those in the model group, the X-ray score, BMD, maximum load and stiffness of the bone, the levels of ALP and osteocalcin in the Cordycepin group increased obviously, the expression levels of COX-2, PGE2, cAMP, and VEGF in the bone tissue increasedobviously, and the level of CTX-Ⅰ reduced obviously (P<0.05). NS-398 reversed the promoting effect of Cordycepin on fracture healing in osteoporosis rats. Conclusion Cordycepin promotes fracture healing in osteoporosis rats by activating COX-2/PGE2 signal pathway.
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