ArticleArchives of Razi Institute2025
Mir‑429 and GATA4 May Participate in Cerebral Ischemic Stroke by Regulating Autophagy and Apoptosis: the Impact of Chlorogenic Acid.
Article in Archives of Razi Institute, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Autophagy is a double-edged sword for maintaining neural system homeostasis during the development of cerebral ischemia. However, the potential molecular mechanisms behind this remain unclear. Changes in miR-429 and its target GATA4, along with autophagy mediators and apoptosis in ischemic stroke, were examined in this research. Additionally, the study investigated these factors in combination with chlorogenic acid (CGA). Male Wistar rats were separated into three categories. (n=8): sham, IR (ischemia-reperfusion, Induction of transient cerebral ischemia via occlusion and reperfusion of the common carotid artery.) and IR+CGA (30 mg/kg, ip; administered intraperitoneally, 10 minutes before the onset of ischemia and 10 minutes prior to reperfusion). Levels of miR-429, GATA4, c-Caspase-3 / p-Caspase-3 ratio, LC3-I, LC3-II, Beclin1 and p62 were assessed using Real- time PCR and Western blot assays. At the end of the experiment, increased miR-429 gene expression (P<0.05) and c-Caspase-3/p-Caspase-3 ratio (P<0.01), along with decreased GATA4 protein expression (P<0.001), were observed in IR group. In addition, the brains of CCAO rats displayed significantly increased autophagy activation, as evidenced by an increased LC3-II/I ratio and Beclin1 protein expression, and decreased p62 expression after 24 h of reperfusion (P<0.001). Immunohistochemistry studies has alsorevealed that the ratio of overall LC3 immunoreactivity in the cortex tissue of male rats was significantly increased by cerebral IR (P<0.001). Treatment with CGA significantly attenuated autophagic activity and apoptosis, reversing the aforementioned molecule levels. Taken together, these results suggested that ischemic insult can increase autophagic activities and apoptosis, possibly through miR‑429 and GATA4 alterations in the brain cortex following cerebral IR insult, which can be alleviated by CGA as a potential therapy for individuals affected by ischemia.
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