Five Constituents in Psoralea corylifolia L. Attenuate Palmitic Acid-Induced Hepatocyte Injury via Inhibiting the Protein Kinase C-α/Nicotinamide-Adenine Dinucleotide Phosphate Oxidase Pathway

Zhou, Ling; Tang, Jianqiao; Yang, Xuan; Xiong, Xiaoli; Huang, Juan; Zhang, Linli; Qin, Huan; Yan, Su-Qi

doi:10.3389/fphar.2019.01589

Cited by 20 publications

(12 citation statements)

References 38 publications

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“…Previous studies have found that apigenin can regulate hepatocyte lipid metabolism and oxidative stress by adjusting PPAR γ [ 31 ], Nrf2 [ 31 ], and XO/NLRP3 pathways [ 32 ], thereby attenuating HFD-induced NAFLD. Psoralen is one of the main components of FV, which has the ability to relieve lipid accumulation in PA-induced primary hepatocyte model of NAFLD through downregulating the intracellular content of TC and TG [ 33 ]. Simultaneously, the 8-methoxypsoralen, a vitamin D receptor ligand with a promising antisteatosis action, can relieve the symptoms of NAFLD by binding to vitamin D receptor [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Ficus hirta Vahl. Ameliorates Nonalcoholic Fatty Liver Disease through Regulating Lipid Metabolism and Gut Microbiota

Quan

Zhou

Chen

et al. 2022

Oxidative Medicine and Cellular Longevity

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Nonalcoholic fatty liver disease (NAFLD) has gradually become one of the most serious liver diseases threatening human health in the world. Currently, Chinese herbal medicine is a potentially important treatment option for NAFLD, and the development of effective Chinese herbal medicine has a good prospect. Previous studies have suggested that Ficus hirta Vahl. (FV) has various protective effects on the liver. In this study, we investigated the therapeutic outcomes of FV treatment for the liver disease and its underlying mechanism using HepG2 cell lines induced by palmitate (PA) and mouse model fed with high-fat diet (HFD). FV mainly exerts pharmacological effects by mediating lipid metabolism and inflammation. During the lipid metabolism regulation process, CD36, SREBP-1, SCD1, PPAR γ, ACOX1, and CPT1α are the key factors related to the healing effects of FV on NAFLD. During the inflammation process, the downregulation of IL-6, IL-1β, and TNF-α is involved in alleviation of NAFLD. Furthermore, CD36 overexpression promotes lipid abnormal metabolism and inflammation in PA-induced HepG2 cells, while CD36 knockdown and FV supplementation reverse these responses. In addition, FV also modulates gut microbiota composition, such as Allobaculum, Faecalibaculum, and Butyricicoccus in HFD-fed mice. In summary, our findings demonstrated that FV exerted a beneficial preventive and therapeutic effect on NAFLD by improving lipid metabolism and inflammation as well as regulating the structure of gut microbiota, and therefore, FV may be a candidate for the treatment of NAFLD.

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Section: Discussionmentioning

confidence: 99%

Ficus hirta Vahl. Ameliorates Nonalcoholic Fatty Liver Disease through Regulating Lipid Metabolism and Gut Microbiota

Quan

Zhou

Chen

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Other studies have shown that the contents of TG and TC in primary hepatocytes of young mice can be reduced after IBC treatment. IBC can improve hepatocyte steatosis, relieve oxidative stress, down‐regulate the PKC‐α/NOX signaling pathway, and alleviate palmitic acid (PA) induced hepatocyte injury (Zhou et al, 2019). Therefore, the toxicity limitations of IBC need to be further studied.…”

Section: Discussion and Perspectivesmentioning

confidence: 99%

Isobavachalcone: A comprehensive review of its plant sources, pharmacokinetics, toxicity, pharmacological activities and related molecular mechanisms

Xing

Meng

Wang

2022

Phytotherapy Research

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Isobavachalcone (IBC), also known as isobapsoralcone, is a natural flavonoid widely derived from many medicinal plants, including Fabaceae, Moraceae, and so forth. IBC has been paid more and more attention by researchers in recent years due to its pharmacological activity in many diseases. This review aims to describe in detail the plant sources, pharmacokinetics, toxicity, pharmacological activities, and molecular mechanisms of IBC on various diseases. We found that IBC can be obtained not only by extraction but also by chemical synthesis. Pharmacokinetic studies have shown that IBC has low bioavailability, but can penetrate the blood–brain barrier and is widely distributed in the brain. Its pharmacological activities mainly include anticancer, antibacterial, anti‐inflammatory, antiviral, neuroprotective, bone protection, and other activities. In particular, IBC shows strong anti‐tumor and anti‐inflammatory therapeutic potential due to its anti‐cancer and anti‐inflammatory activities. However, due to its hepatotoxicity, there may be more drug interactions. Therefore, more and more in‐depth studies are needed for its clinical application. Mechanically, IBC can induce the production of reactive oxygen species (ROS), inhibit AKT, ERK, and Wnt pathways, and promote apoptosis of cancer cells through mitochondrial or endoplasmic reticulum pathways. IBC can inhibit the NF‐κB pathway and the production of multiple inflammatory mediators by activating NRF2/HO‐1 pathway, thus producing anti‐inflammatory effects. Moreover, we discussed the limitations of current research on IBC and put forward some new perspectives and challenges, which provide a strong basis for clinical application and new drug development of IBC in the future.

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“…It has been shown that LPS treatment or HFD feeding can cause inflammation and increased cholesterol concentration in mouse livers [ 30 , 31 ]. In recent years, many studies also have demonstrated that treatment with low levels of LPS or PA for a long period of time can activate the TLR4 inflammatory signaling pathway and lead to chronic inflammation [ 15 , 38 ], which promotes cholesterol accumulation in L02 cells, Huh7 cells, primary hepatocytes, and THP-1 macrophages [ 5 , 39 , 40 , 41 , 42 ]. Similar results were obtained in this study.…”

Section: Discussionmentioning

confidence: 99%

Inflammation Induced by Lipopolysaccharide and Palmitic Acid Increases Cholesterol Accumulation via Enhancing Myeloid Differentiation Factor 88 Expression in HepG2 Cells

Chen

Luo

et al. 2022

Pharmaceuticals

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Recently, multiple studies have shown that chronic inflammation disturbs cholesterol homeostasis and promotes its accumulation in the liver. The underlying molecular mechanism remains to be revealed. The relationship between the toll-like receptor 4 (TLR4) inflammatory signaling pathway and cholesterol accumulation was investigated in HepG2 cells treated with lipopolysaccharide (LPS) or palmitic acid (PA) for different lengths of time. In addition, the effects of pretreatment with 20μmol/L ST2825 (MyD88 inhibitor) were also studied in LPS- or PA-treated HepG2 cells and myeloid differentiation factor 88 (MyD88)-overexpressing HEK293T cells. The intracellular total and free cholesterol levels were measured using a commercial kit and filipin staining, respectively. The expression levels of sterol regulatory element-binding protein-2 (SREBP-2) and components in the TLR4 signaling pathway were determined using Western blotting. The treatments with LPS for 12 h and with PA for 24 h significantly increased the contents of intracellular total and free cholesterol, as well as the expression levels of SREBP-2 and components in the TLR4 signaling pathway. The inhibition of MyD88 by ST2825 significantly decreased the cholesterol content and the expression levels of SREBP-2 and components of the TLR4/MyD88/NF-κB pathway in HepG2 cells, as well as MyD88-overexpressing HEK293T cells. These results indicated that LPS and PA treatments increase SREBP-2-mediated cholesterol accumulation via the activation of the TLR4/MyD88/NF-κB signaling pathway in HepG2 cells.

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Five Constituents in Psoralea corylifolia L. Attenuate Palmitic Acid-Induced Hepatocyte Injury via Inhibiting the Protein Kinase C-α/Nicotinamide-Adenine Dinucleotide Phosphate Oxidase Pathway

Cited by 20 publications

References 38 publications

Ficus hirta Vahl. Ameliorates Nonalcoholic Fatty Liver Disease through Regulating Lipid Metabolism and Gut Microbiota

Ficus hirta Vahl. Ameliorates Nonalcoholic Fatty Liver Disease through Regulating Lipid Metabolism and Gut Microbiota

Isobavachalcone: A comprehensive review of its plant sources, pharmacokinetics, toxicity, pharmacological activities and related molecular mechanisms

Inflammation Induced by Lipopolysaccharide and Palmitic Acid Increases Cholesterol Accumulation via Enhancing Myeloid Differentiation Factor 88 Expression in HepG2 Cells

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