Histology and histopathology · 2025
Pinocembrin ameliorates non-alcoholic fatty liver disease by activating Nrf2/HO-1 and inhibiting the NF-κB signaling pathway.
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Chen Weina, Xue Diming, Feng Xia, Zhong Yinhang, Li Quanqing, Zhang Weihang, Jiang Guojun
Аннотация
OBJECTIVES: The high intake of high-fat diets and changes in sedentary lifestyles have led to an increase in non-alcoholic fatty liver disease (NAFLD). This study aimed to investigate the effect and mechanism of Pinocembrin (Pin) on NAFLD in vivo and in vitro.
METHODS: The pharmacodynamics of Pin alone or in combination with ML385 was assessed in high-fat diet (HFD)-mediated NAFLD mice. HepG2 cells were treated with palmitic acid (PA)/oleic acid (OA) (1:2) as an in-vitro model to study the effect of Pin on lipid deposition and oxidative stress. The roles of Pin in glucose and lipid metabolism, inflammation, oxidative stress, and the Nrf2/HO-1/NF-κB pathway were measured.
RESULTS: Pin alleviated lipid deposition, inflammatory response, and oxidative stress in HFD-induced NAFLD mice and PA/OA-induced HepG2 cells. Moreover, ML385 partly attenuated the protection of Pin on inflammatory response and oxidative stress in vivo and in vitro. More importantly, feeding with an HFD significantly decreased the expression of Nrf2 and HO-1, but treatment with Pin increased their expression, accompanied by an increased nuclear transposition of Nrf2.
CONCLUSION: Taken together, these results indicated that Pin alleviated glucose and lipid metabolism disorders, inflammation, and oxidative stress in NAFLD by activating the Nrf2/HO-1 signaling pathway and restraining the NF-κB pathway.
METHODS: The pharmacodynamics of Pin alone or in combination with ML385 was assessed in high-fat diet (HFD)-mediated NAFLD mice. HepG2 cells were treated with palmitic acid (PA)/oleic acid (OA) (1:2) as an in-vitro model to study the effect of Pin on lipid deposition and oxidative stress. The roles of Pin in glucose and lipid metabolism, inflammation, oxidative stress, and the Nrf2/HO-1/NF-κB pathway were measured.
RESULTS: Pin alleviated lipid deposition, inflammatory response, and oxidative stress in HFD-induced NAFLD mice and PA/OA-induced HepG2 cells. Moreover, ML385 partly attenuated the protection of Pin on inflammatory response and oxidative stress in vivo and in vitro. More importantly, feeding with an HFD significantly decreased the expression of Nrf2 and HO-1, but treatment with Pin increased their expression, accompanied by an increased nuclear transposition of Nrf2.
CONCLUSION: Taken together, these results indicated that Pin alleviated glucose and lipid metabolism disorders, inflammation, and oxidative stress in NAFLD by activating the Nrf2/HO-1 signaling pathway and restraining the NF-κB pathway.