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[1]李桂林,鄧琳,羅金英,等.鐵死亡在新生大鼠高膽紅素血癥腦損傷中的作用[J].福建醫(yī)藥雜志,2023,45(04):97-101.
 LI Guilin,DENG Lin,LUO Jinying,et al.Role of ferroptosis in hyperbilirubinemia induced brain injury in neonatal rats[J].FUJIAN MEDICAL JOURNAL,2023,45(04):97-101.
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鐵死亡在新生大鼠高膽紅素血癥腦損傷中的作用()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
45
期數(shù):
2023年04期
頁碼:
97-101
欄目:
基礎(chǔ)研究
出版日期:
2023-08-15

文章信息/Info

Title:
Role of ferroptosis in hyperbilirubinemia induced brain injury in neonatal rats
文章編號:
1002-2600(2023)04-0097-05
作者:
李桂林鄧琳羅金英周進(jìn)福1
福建省婦幼保健院 福建醫(yī)科大學(xué)婦兒臨床醫(yī)學(xué)院(福州 350003)
Author(s):
LI Guilin DENG Lin LUO Jinying ZHOU Jinfu
Fujian Maternity and Child Health Hospital, College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian 350001, China
關(guān)鍵詞:
高膽紅素血癥 腦損傷 鐵死亡 ACSL4
Keywords:
hyperbilirubinemia brain injury ferroptosis ACSL4
分類號:
R332; R722
文獻(xiàn)標(biāo)志碼:
A
摘要:
目的 探究鐵死亡在新生大鼠高膽紅素血癥腦損傷中的作用。方法 通過腹腔注射鹽酸苯肼構(gòu)建高膽紅素血癥腦損傷動物模型,應(yīng)用鐵死亡抑制劑及鐵鰲合劑去鐵胺干預(yù),檢測神經(jīng)元特異性烯醇化酶(NSE)、S100鈣結(jié)合蛋白B(S100B)、腦組織鐵、氧化應(yīng)激損傷、鐵死亡生化指標(biāo)和鐵死亡通路的關(guān)鍵蛋白。結(jié)果 與對照組相比,實(shí)驗組血清腦損傷分子標(biāo)志物NSE和S100B水平明顯升高、腦組織氧化應(yīng)激及鐵死亡生化指標(biāo)GSH水平下降、MDA水平升高、組織鐵水平升高和SOD活性降低,差異具有統(tǒng)計學(xué)意義(P<0.05),在應(yīng)用去鐵胺干預(yù)后,可逆轉(zhuǎn)上述指標(biāo)的改變。與對照組相比,實(shí)驗組鐵死亡通路的關(guān)鍵蛋白ACSL4表達(dá)上調(diào),而FSP1表達(dá)下調(diào),GPX4在實(shí)驗組中表達(dá)上調(diào),差異具有統(tǒng)計學(xué)意義(P< 0.05),DFO干預(yù)后可逆轉(zhuǎn)上述改變。結(jié)論 鐵死亡參與新生高膽紅素血癥大鼠腦損傷,為膽紅素神經(jīng)毒性機(jī)制研究提供新思路,但其具體機(jī)制有待于進(jìn)一步闡明。
Abstract:
Objective To explore the role of ferroptosis in hyperbilirubinemia induced brain injury in neonatal rats. Methods An animal model of hyperbilirubinemia induced brain injury was established by intraperitoneal injection of phenylhydrazine hydrochloride. An animal model of hyperbilirubinemia was intervented with deferoxamine, which was known as ferroptosis inhibitors and iron chelation. NSE, S100B, tissue iron, biochemical indicators and key proteins of pathway of ferroptosis were determined. Results Compared with the control group, the serum levels of NSE and S100 B, which were the markers of brain injury, increased in the experimental group(P<0.05). Compared with the control group, the level of GSH decreased,MDA increased, SOD activity decreased, and tissue iron increased in the experimental group(P<0.05). Western blot results showed that compared with the control group, the expression protein of ACSL4 and GPX4 increased in the brain tissue of the rats in the experimental group, while the expression protein of FSP1 decreased(P<0.05). DFO intervention could partially or completely reverse the changes of the above biomarker in rats with hyperbilirubinemia induced brain injury. Conclusion Ferroptosis is involved in hyperbilirubinemia induced brain injury in neonatal rats, which provids a new idea for the mechanism of bilirubin neurotoxicity. However, the specific mechanism of ferroptosis participated in bilirubin neurotoxicity needs to be further clarified.

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備注/Memo

備注/Memo:
基金項目:福建省自然科學(xué)基金面上項目(2020J01327); 福建省衛(wèi)生健康委中青年骨干人才培養(yǎng)項目(2020GGB017)
1 通信作者,Email:[email protected]
更新日期/Last Update: 2023-08-15