Pravastatin ameliorated osteoarthritis susceptibility in male offspring rats induced by prenatal ethanol exposure
Pravastatin ameliorated osteoarthritis susceptibility in male offspring rats induced by prenatal ethanol exposure
复制标题
普伐他汀改善了产前乙醇暴露引起的雄性子代大鼠的骨关节炎易感性。
DOI：
10.1016/j.bone.2021.115976
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发表时间：
2021-04-28
期刊：
影响因子：
4.1
通讯作者：
Chen, Liaobin
中科院分区：
文献类型：
--
作者：
Ni, Qubo;Chen, Haitao;Chen, Liaobin
Osteoarthritis (OA) is a disease associated with a disorder of cholesterol metabolism. Our previous studies showed that prenatal ethanol exposure (PEE) caused cholesterol accumulation in articular cartilage and increased the susceptibility to OA in offspring. However, we did not determine whether pravastatin, a cholesterol-lowering agent, could rescue PEE-induced susceptibility to OA. Here, fetal rats were divided into a PEE group and a control group during pregnancy. At postnatal week (PW) 8, sixteen male offspring rats from both groups were injected papain through the articular cavity. Eight of them from each group were treated with pravastatin (20 mg/kg.d) by gavage for four weeks simultaneously. We found that pravastatin ameliorated papain-induced high expression of inflammatory factors [interleukin (IL)-1, IL-6], matrix degradation enzymes [matrix metalloproteinase (MMP)-3, MMP-13], and apoptosis factors (caspase-3 and caspase-8) in the cartilage of the PEE group. Also, pravastatin significantly reduced the content of TCH in the blood and cartilage of the PEE offspring and improved cholesterol efflux pathway. Our in vitro findings further confirmed that pravastatin partially reversed cholesterol-induced inflammation and apoptosis of chondrocytes. In conclusion, pravastatin effectively reduced inflammation and matrix degradation, and thus ameliorate OA susceptibility in articular cartilage by relieving cholesterol accumulation in chondrocyte.
