Li Xiaoya, Li Ning, Pei Huan, Ren Yu, Li Lei, Sun Lan, Wu Yueying, Yuan Jiali, Ma Yuan
School of Basic Medical Sciences, Yunnan University of Chinese Medicine, Kunming, Yunnan, China.
Yunnan Provincial Key Laboratory of Integrated Traditional Chinese and Western Medicine for Chronic Disease in Prevention and Treatment, Yunnan University of Chinese Medicine, Kunming, Yunnan, China.
Front Cell Infect Microbiol. 2024 Dec 4;14:1500111. doi: 10.3389/fcimb.2024.1500111. eCollection 2024.
Zhuanggu Shubi ointment (ZGSBG) has good efficacy in postmenopausal osteoporosis (PMO), but the mechanism of efficacy involving gut microecology has not been elucidated.
This study investigated the mechanism of ZGSBG in regulating gut microecology in PMO.
The bilateral ovarian denervation method was used to construct a rat model of PMO and was administered ZGSBG. Behavior, bone transformation, gut microbiota, intestinal mucosal barrier, and intestinal inflammatory-related indexes were detected.
After ZGSBG intervention, bone R-hydroxy glutamic acid protein and procollagen type I N-terminal propeptides were significantly upregulated, while C-terminal telopeptide of type-I collagen and tartrate-resistant acid phosphatase-5b were significantly downregulated. Pathological analysis demonstrated an improvement in femoral and colonic structures. The expressions of zonula occludens-1, occludin, claudin-1, and secretory immunoglobulin A in the colonic tissues were significantly elevated, while the levels of tumor necrosis factor-α, interleukin-1β, interleukin-6, and lipopolysaccharides were reduced. Moreover, characteristic bacteria and were significantly enriched. Furthermore, and have a positive correlation with intestinal mucosal barrier function and a negative correlation with intestinal inflammatory responses.
ZGSBG promoted bone formation, inhibited bone resorption, regulated gut microbiota, repaired intestinal mucosal barrier damage, and inhibited intestinal inflammatory responses in PMO rats. and might play positive roles in ZGSBG treatment of intestinal mucosal barrier injury and inflammatory reactions in PMO.
壮骨疏痹膏(ZGSBG)在绝经后骨质疏松症(PMO)中具有良好疗效,但涉及肠道微生态的作用机制尚未阐明。
本研究探讨ZGSBG调节PMO大鼠肠道微生态的作用机制。
采用双侧卵巢去神经法构建PMO大鼠模型,并给予ZGSBG干预。检测大鼠行为、骨转化、肠道微生物群、肠黏膜屏障及肠道炎症相关指标。
ZGSBG干预后,骨R-羟基谷氨酸蛋白和I型前胶原N端前肽显著上调,而I型胶原C端肽和抗酒石酸酸性磷酸酶-5b显著下调。病理分析显示股骨和结肠结构有所改善。结肠组织中紧密连接蛋白-1、闭合蛋白、Claudin-1和分泌型免疫球蛋白A的表达显著升高,而肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-6和脂多糖水平降低。此外,特征菌[具体菌名缺失]和[具体菌名缺失]显著富集。此外,[具体菌名缺失]和[具体菌名缺失]与肠黏膜屏障功能呈正相关,与肠道炎症反应呈负相关。
ZGSBG可促进PMO大鼠骨形成、抑制骨吸收、调节肠道微生物群、修复肠黏膜屏障损伤并抑制肠道炎症反应。[具体菌名缺失]和[具体菌名缺失]可能在ZGSBG治疗PMO肠黏膜屏障损伤和炎症反应中发挥积极作用。