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Archive > Volume 15 Issue 2 > 2023,15(2):231-239. DOI:https://doi.org/10.1016/j.chmed.2023.01.002 Prev Next

和厚樸酚通過抑制肝臟CYP1A2活性和改善肝臟線粒體功能障礙來減輕對(duì)乙酰氨基酚引起的急性肝損傷

Original articles

Honokiol attenuates acetaminophen-induced acute liver injury by inhibiting hepatic CYP1A2 activity and improving liver mitochondrial dysfunction

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    摘要:
    目的 對(duì)乙酰氨基酚（APAP）過量是導(dǎo)致肝臟損傷的常見原因。本研究旨在探討Honokiol（Hon）對(duì)APAP引起的肝臟毒性的保護(hù)作用及其潛在機(jī)制。方法 C57BL/6小鼠在腹腔注射APAP（300mg/kg）后，腹腔注射Hon（10和30mg/kg）。在Hon治療后1.5小時(shí)和5小時(shí)，收集血清和肝臟。然后評(píng)估肝臟損傷相關(guān)指標(biāo)、APAP代謝相關(guān)指標(biāo)、線粒體呼吸鏈功能相關(guān)指標(biāo)和線粒體膜功能相關(guān)蛋白表達(dá)。結(jié)果 發(fā)現(xiàn)Hon明顯降低了血清ALT/AST活性和GSH消耗，提高了肝臟CAT和GPx活性，降低了肝臟MDA和3-硝基酪氨酸含量，抑制了肝臟CYP1A2活性和APAP蛋白加合物（APAP-CYS）形成。同時(shí)，Hon處理后，線粒體呼吸鏈中復(fù)合物I的氧化磷酸化能力和復(fù)合物IV的電子轉(zhuǎn)移能力增加，而線粒體中過氧化氫的釋放減少。此外，Hon明顯降低了細(xì)胞質(zhì)和線粒體中的P-JNK，并明顯抑制了AIF和EndoG從線粒體到細(xì)胞質(zhì)的釋放。結(jié)論 Hon通過以下途徑減輕了APAP誘導(dǎo)的肝臟損傷：通過抑制CYP1A2的活性減少APAP-CYS的產(chǎn)生；通過提高肝臟CAT、GPx和GSH的水平改善肝臟氧化應(yīng)激；通過促進(jìn)復(fù)合物I的氧化磷酸化能力和復(fù)合物IV的電子轉(zhuǎn)移能力改善線粒體呼吸鏈功能；通過抑制P-JNK及其向線粒體的轉(zhuǎn)位改善線粒體的功能，從而減少AIF和EndoG的釋放

    Abstract:
    Objective: Acetaminophen (APAP) overdose is a common cause of liver injury. This study aimed to investigate the protective effect of honokiol (Hon) against APAP-induced hepatotoxicity and its potential mechanism. Methods: C57BL/6 mice were administrated with Hon (10 and 30 mg/kg) after APAP (300 mg/kg) treatment. On 1.5 h and 5 h after Hon treatment, mice were sacrificed. Serum and liver were collected. And then, liver injury-related indexes, APAP metabolism-related indexes, mitochondrial respiratory chain function-related indexes, and mitochondrial membrane function-related protein expression were evaluated. Results: It was found that Hon significantly decreased serum alanine aminotransferase (ALT)/aspartate aminotransferase (AST) activity and glutathione (GSH) depletion, increased hepatic catalase (CAT) and GSH peroxidase (GSH-Px) activities, reduced hepatic MDA and 3-nitrotyrosine contents, inhibited hepatic CYP1A2 activity and APAP protein adducts (APAP-CYS) formation. Meanwhile, oxidative phosphorylation capacity of complex I and electron transfer capacity of complex IV in mitochondrial respiratory chain was increased, whereas the release of H2O2 in the mitochondria was decreased following Hon treatment. Furthermore, Hon markedly down-regulated p-JNK in both cytosol and mitochondria, and obviously inhibited the release of apoptosis inducing factor (AIF) and endonuclease G (EndoG) from mitochondria to cytosol. Conclusion: Hon alleviated APAP-induced liver injury through the following pathways: Reducing the production of APAP-CYS by inhibiting CYP1A2 activity; Ameliorating hepatic oxidative stress by increasing the levels of hepatic CAT, GSH-Px and GSH; Improving mitochondrial respiratory chain function by promoting oxidative phosphorylation capacity of complex I and electron transfer capacity of complex IV; Improving the function of mitochondrial membrane by inhibiting p-JNK and its translocation to mitochondria, thereby reducing the release of AIF and EndoG

    關(guān)鍵詞:
    對(duì)乙酰氨基酚;CYP1A2; 和厚樸酚; 肝臟線粒體功能紊亂; 厚樸;氧化應(yīng)激

    Keywords:


    Project Supported:
    This work was supported by the Department of Education of Hubei Province, China (No. Q20181004).

    Clc Number:

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