[Chrysin alleviates cerebral ischemia-reperfusion injury by inhibiting ferroptosis in rats].

• DOI: 10.19540/j.cnki.cjcmm.20221201.705
• Publication Date: 2023-03-01
• Authors: Jinfeng Shang; Jiakang Jiao; Qiannan Li; Yinghui Lü; Jingyi Wang; Ming-Xue Yan; Yin-Lian Wen; Gui-Jin-Feng Huang; Xiaolu Zhang; Xin Liu
• Keywords: Nissl body; Chrysin; Malondialdehyde

The purpose of this study is to investigate whether chrysin reduces cerebral ischemia-reperfusion injury(CIRI) by inhi-biting ferroptosis in rats. Male SD rats were randomly divided into a sham group, model high-, medium-, and low-dose groups(200, 100, 50 mg·kg~(-1)), positive drug group(Ginaton, 21.6 mg·kg~(-1)). CIRI was induced transient middle artery occlusion(tMCAO). indexes evaluated the samples taken 24 h after operation. neurological deficit score used detect function. 2,3,5-triphenyl tetrazolium chloride(TTC) staining infarction area. Hematoxylin-eosin(HE) Nissl observe morphological structure brain tissues. Prussian blue iron accumulation brain. Total iron, lipid pero-xide, malondialdehyde serum tissues detected biochemical reagents. Real-time quantitative polymerase chain reaction(RT-qPCR), immunohistochemistry, Western blot mRNA protein expression solute carrier fa-mily 7 member 11(SLC7A11), transferrin receptor 1(TFR1), glutathione peroxidase 4(GPX4), acyl-CoA synthetase long family 4(ACSL4), prostaglandin-endoperoxide synthase 2(PTGS2) Compared with groups intervention showed restored function, decreased rate, alleviated pathological changes. group selected as optimal dosing group. reduced content total peroxide, serum, increased levels SLC7A11 GPX4, TFR1, PTGS2, ACSL4. Chrysin may regulate metabolism via regulating related targets inhibit neuronal CIRI.