| ORIGINAL ARTICLE |
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| Year : 2020 | Volume
: 16
| Issue : 67 | Page : 177-182 |
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Propionic acid abrogates the deleterious effects of cerebral ischemic reperfusion injury through nuclear factor-κb signaling in mice
Tiansong Yang1, Yulin Wang2, Chaoran Li2, Yan Yang2, Delong Wang2, Jing Guo2, Tianyu Shi2, Yue Wang2, Yuanyuan Qu2, Qingshuang Wei2, Chuwen Feng2, Zhongren Sun2
1 Department of Neurology, First Affiliated Hospital, Heilongjiang University of Chinese Medicine, Heilongjiang, China
2 Heilongjiang University of Chinese Medicine, Xiangfang District, Harbin, Heilongjiang, China
Correspondence Address:
Zhongren Sun
Heilongjiang University of Chinese Medicine, No.26, Heping Road, Xiangfang District, Harbin 150040, Heilongjiang
China
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/pm.pm_306_19
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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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