缺血
细胞凋亡
药理学
一氧化氮合酶
免疫印迹
医学
肿瘤坏死因子α
再灌注损伤
一氧化氮
白细胞介素
化学
内分泌学
免疫学
内科学
细胞因子
生物化学
基因
作者
Tiansong Yang,Yulin Wang,Chaoran Li,Yan Yang,Delong Wang,Jing Guo,Tianyu Shi,Yue Wang,Yuanyuan Qu,Qingshuang Wei,Chuwen Feng,Zhongren Sun
摘要
Background: Cerebral ischemia is caused due to insufficient blood flow to brain cells. This study evaluates the therapeutic effects of propionic acid (PA) on the abnormalities induced during the cerebral ischemic-reperfusion (CIR) injury in mice. Materials and Methods: CIR was induced by complete occlusion of the middle artery of the cerebrum for 15 min and reperfusion for 24 h in the experimental C57BL/6 mice. The analysis of mRNA levels of neuronal nitric oxide synthase (nNOS) was performed by reverse transcriptase polymerase chain reaction (RT-PCR). Inflammatory cytokines such as interleukin-6 (IL-6), IL-1 β, and tumor necrosis factor-alpha were quantitated by enzyme-linked immuno sorbent assay. Apoptosis-related proteins and nuclear factor-κB (NF-κB) were analyzed using Western blot technique. Results: PA demonstrated strong therapeutic effects on controlling the expression of nNOS that was analyzed using RT-PCR. Elevated levels of inflammatory cytokines, caspase-3, caspase-9, and phosphorylated NF-κB during cerebral ischemia were significantly controlled during PA treatment. Conclusion: Our findings demonstrated that PA through oral gavage exhibited healthier effects on the damage caused due to CIR injury.
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