益生菌制剂通过PI3K/Akt信号通路改善骨质疏松大鼠的骨代谢和骨量
Probiotic preparations improve bone metabolism and bone mass in osteoporotic rats through PI3K/Akt signaling pathway
  
DOI:10.3969/j.issn.1006-7108.2022.08.009
中文关键词:  骨质疏松症  益生菌制剂  肠道菌群失调  PI3K/AKT通路  骨代谢  骨量
英文关键词:osteoporosis  probiotics  intestinal flora imbalance  PI3K/AKT pathway  bone metabolism  bone mass
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刘旭良1* 周元敏2 曾祥英3 王兆杰1 宋慧东4 李伯庭1 1 广州市第十二人民医院骨外科 2 广州市第十二人民医院放射科 3 广州市第十二人民医院供应室 4 广州市第十二人民医院消化内科 
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中文摘要:
      摘要:目的 从磷脂酰肌醇3激酶/丝氨酸-苏氨酸激酶(PI3K/AKT)通路,观察肠道菌群调节剂-益生菌制剂对骨代谢及骨量的影响,为益生菌治疗骨质疏松症(osteoporosis,OP)提供可靠资料。方法 建立肠道菌群失调性OP大鼠模型,并设置为正常对照组、模型组、益生菌制剂组、PI3K/AKT通路激活剂组、益生菌制剂+通路激活剂组,每组15只。给药干预治疗14 d后,检测粪便含水量及菌群分布;通过ELISA法检测血清炎症因子及骨生物学指标变化、骨密度仪检测骨密度、灰化法检测骨灰重、HE及抗酒石酸酸性磷酸酶(TRACP)染色观察骨病理损伤及破骨细胞骨吸收数目、Western blot法检测PI3K/Akt通路相关蛋白表达。结果 与正常对照组相比,模型组大鼠肠道菌群失衡,血清炎症因子升高,骨代谢异常(促骨形成因子减少,β-CTX及RANKL等破骨活性降低),PI3K/Akt通路活性升高(P<0.05)。益生菌制剂可纠正肠道菌群失衡,抑制血清炎症因子释放、改善OP大鼠骨代谢失衡,并抑制PI3K/Akt通路活性(P<0.05)。PI3K/Akt通路激活剂可削弱益生菌制剂的上述作用,加重骨代谢失衡及肠道菌群失调(P<0.05)。结论 益生菌制剂干预治疗,可减弱菌群失调并纠正OP大鼠的骨代谢异常,且其作用可能与抑制PI3K/Akt通路激活有关。
英文摘要:
      Abstract: Objective From the phosphatidylinositol 3-kinase/serine-threonine kinase (PI3K/AKT) pathway, to observe the effects of intestinal flora regulator-probiotic preparations on bone metabolism and bone mass, and to provide reliable information for probiotics to treat osteoporosis (OP). Methods The intestinal flora dysbiosis OP model was established and set as: normal control group, model group, probiotic preparation group, PI3K/AKT pathway activator group, probiotic preparation + pathway activator group, with 15 animals in each group. After 14 days of drug intervention, the water content and flora distribution of feces were detected; the changes of serum inflammatory factors and bone biological indexes were detected by ELISA; the bone mineral density was detected by absorptiometry; (TRACP) staining was used to observe the number of bone pathological damage and osteoclast bone resorption; Western blot was used to detect the expression of PI3K/Akt pathway-related proteins. Results Compared with the normal control group, the rats in the model group showed an imbalance of intestinal flora, increased serum inflammatory factors, abnormal bone metabolism (decreased osteogenesis factors, decreased osteoclastic activities such as β-CTX and RANKL), and PI3K/Akt pathway. The activity increased (P<0.05). Probiotic preparations can correct the imbalance of intestinal flora, inhibit the release of serum inflammatory factors, improve the imbalance of bone metabolism in OP rats, and inhibit the activity of PI3K/Akt pathway (P<0.05). PI3K/Akt pathway activators can weaken the above effects of probiotic preparations, aggravate the imbalance of bone metabolism and intestinal flora in OP (P<0.05) Conclusion Intervention treatment with probiotic preparations can attenuate the dysbacteriosis of rats and correct the abnormal OP bone metabolism, and its effect may be related to the inhibition of PI3K/Akt pathway activation.
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