姜黄素通过 SIRT3 通路改善出生后过度喂养大鼠和脂肪 L02 细胞的线粒体功能，从而减轻肝脂肪变性,Food & Function

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姜黄素通过 SIRT3 通路改善出生后过度喂养大鼠和脂肪 L02 细胞的线粒体功能，从而减轻肝脂肪变性
Food & Function ( IF 5.1 ) Pub Date : 2022-02-03 , DOI: 10.1039/d1fo03752h
Susu Du ₁ , Xiaolei Zhu ₁ , Nan Zhou ₁ , Wen Zheng ₁ , Wei Zhou ₁ , Xiaonan Li _{1,

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Affiliation

产后过度喂养可能会增加成年期非酒精性脂肪肝（NAFLD）的风险。本研究调查了姜黄素 (CUR) 对产后过度喂养大鼠肝脏脂肪变性的影响，并阐明了线粒体功能的潜在机制。雄性大鼠在出生后第 3 天调整为 10 只（正常窝，NL）或 3 只（小窝，SL）。断奶后，给 NL 大鼠喂食正常饮食（NL）或高脂饮食（NH）10 周. SL大鼠分别饲喂正常饮食（SL）、高脂饮食（SH）、补充2% CUR的正常饮食（SL-CUR）或补充2% CUR的高脂饮食（SH-CUR）。13周时，与NL大鼠相比，SL和NH大鼠出现体重增加、糖耐量异常、血脂异常和肝脏脂质蓄积，这些变化在SH大鼠中更为明显。在 SL-CUR 和 SH-CUR 大鼠中观察到相反的趋势。此外，CUR 可以保护出生后过度喂养大鼠的线粒体生物发生和抗氧化反应，并上调 SIRT3 的 mRNA 和蛋白水平。在体外，L02 细胞暴露于游离脂肪酸和/或 CUR。CUR 降低了细胞脂质和线粒体活性氧的水平，并增加了脂肪 L02 细胞中的线粒体 DNA 拷贝数和超氧化物歧化酶活性。然而，这些效应在 SIRT3 沉默后被阻断。得出的结论是，产后过度喂养损害了线粒体生物合成和抗氧化反应，并增加了肝脂质和高脂诱导的 NAFLD 的严重程度，而 CUR 通过 SIRT3 增强线粒体功能至少部分缓解了肝脂肪变性。

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Curcumin alleviates hepatic steatosis by improving mitochondrial function in postnatal overfed rats and fatty L02 cells through the SIRT3 pathway

Postnatal overfeeding could increase the risk of non-alcoholic fatty liver disease (NAFLD) in adulthood. This study investigated the effects of curcumin (CUR) on hepatic steatosis in postnatal overfed rats and elucidated potential mechanisms in mitochondrial functions. Male rats were adjusted to ten (normal litter, NL) or three (small litter, SL) at postnatal day 3. After weaning, NL rats were fed with normal diet (NL) or a high-fat diet (NH) for 10 weeks. SL rats were fed with normal diet (SL), a high-fat diet (SH), a normal diet supplemented with 2% CUR (SL-CUR) or a high-fat diet supplemented with 2% CUR (SH-CUR). At week 13, compared with NL rats, SL and NH rats showed increased body weight, glucose intolerance, dyslipidemia and hepatic lipid accumulation, and these changes were more obvious in SH rats. The opposite trends were observed in SL-CUR and SH-CUR rats. Moreover, CUR could preserve mitochondrial biogenesis and antioxidant response in postnatal overfed rats, and upregulated the mRNA and protein levels of SIRT3. In vitro, L02 cells were exposed to free fatty acids and/or CUR. CUR decreased the levels of cellular lipids and mitochondrial reactive oxygen species, and increased the mitochondrial DNA copy number and superoxide dismutase activity in fatty L02 cells. However, these effects were blocked after SIRT3 silencing. It was concluded that postnatal overfeeding damaged mitochondrial biogenesis and antioxidant response, and increased hepatic lipids and the severity of high-fat-induced NAFLD, while CUR alleviated hepatic steatosis, at least partially, by enhancing mitochondrial function through SIRT3.

更新日期：2022-02-03

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