Probiotic Lactobacillus Acidophilus prevents bone loss in aged osteoporosis in rats; the possible implication of NLRP3 Inflammasome

M. Allam, Hala Anwer, W. E. El Gazzar, N. Ahmed, N. El-shaer
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Abstract

Senile osteoporosis (SOP) is a degenerative bone disease associated with increasing susceptibility to fractures and mortality in the elderly. Innate immunity and specifically the nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, with its subsequent mediators caspase1-and interlukin-1b (IL-1b),have recently been linked to osteoporosis. Probiotic lactobacillus acidophilus (L.A) was reported to exert favorable effects on osteoporosis. The aim of this study was to identify the protective effects of probiotic L.A in aged osteoporotic rat model and to evaluate the possible underlying mechanisms focusing on NLRP3 inflammasome and its effectors caspase-1 and interleukin -1b. Thirty-two adult male albino rats were designated to four equivalent groups. Group I; control, group II; probiotic L.A, group III; osteoporotic group, and group IV; probiotic LA+ osteoporosis group. Osteoporotic rats pretreated with L.A in a dose of 10 9 CFU/ml / day for 8 weeks revealed a significantly lower oxidative stress state, increased bone mineral density (BMD), enhanced bone histological architecture, lower serum calcium, higher bone formation markers associated with lower bone resorption marker, lower serum receptor activator of nuclear factor kappa- Β ligand (RANKL), decreased bone NLRP3 inflammasome as well as caspase-1 expression levels and lower serum IL-1b.Osteoprotective effects of probiotic L.A in SOP rat model mediated even in part via its anti-inflammatory effects that was represented by decreased NLRP3 inflammasome and its subsequent mediators caspase-1 and IL-1b, that resulted in enhancement of bone formation and reduction of bone resorption.
益生菌嗜酸乳杆菌预防老年骨质疏松大鼠骨质流失;NLRP3炎性体的可能含义
老年性骨质疏松症(SOP)是一种退行性骨病,与老年人骨折易感性和死亡率增加有关。先天免疫,特别是含有3 (NLRP3)炎性体的核苷酸结合寡聚化结构域(NOD)样受体家族pyrin结构域,及其随后的介质caspase1和interleukin -1b (IL-1b),最近与骨质疏松症有关。据报道,益生菌嗜酸乳杆菌(L.A)对骨质疏松症有良好的作用。本研究旨在确定益生菌L.A对老年骨质疏松大鼠模型的保护作用,并以NLRP3炎症小体及其效应物caspase-1和白细胞介素-1b为重点,评估其可能的潜在机制。32只成年雄性白化大鼠被分为四个相等的组。组我;对照组,第二组;益生菌L.A, III组;骨质疏松组和IV组;LA+骨质疏松组。以10 9 CFU/ml /天的剂量L.A预处理骨质疏松大鼠,连续8周,其氧化应激状态显著降低,骨密度(BMD)升高,骨组织结构增强,血清钙水平降低,骨形成标志物升高,骨吸收标志物降低,血清核因子κ - Β配体受体激活物(RANKL)降低,骨NLRP3炎性体和caspase-1表达水平降低,血清IL-1b降低。益生菌L.A在SOP大鼠模型中的骨保护作用甚至部分是通过其抗炎作用介导的,其表现为NLRP3炎性体及其随后的介质caspase-1和IL-1b的减少,从而促进骨形成和减少骨吸收。
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