Propionic Acid Abrogates the Deleterious Effects of Cerebral Ischemic Reperfusion Injury through Nuclear Factor‑κb Signaling in Mice

Abstract

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.

Keywords: Apoptosis; caspase‑3; caspase‑9; cerebral ischemia; inflammatory cytokines; neuronal nitric oxide synthase; nuclear factor‑κB; reperfusion injury