Progress in the treatment of drug-induced liver injury with natural products

Sun, Yuan-kai; Zhang, Yafei; Xie, Li; Ren, F.; Zhu, Xing-yu; Xie, Jing; Zhou, Huan; Xu, Tao

doi:10.1016/j.phrs.2022.106361

Cited by 41 publications

(14 citation statements)

References 175 publications

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“…Natural products are effective in treating AILI, often exerting therapeutic effects through attenuating cellular damage caused by oxidative stress, activating the Nrf2 signaling pathway, reducing the release of inflammatory factors, and regulating GSH synthesis, coupling, and excretion (Sun et al, 2022). Astaxanthin (ASX) is a ketocarotenoid with more potent antioxidant activity than other carotenoids (Ambati et al, 2014).…”

Section: Management Of Ailimentioning

confidence: 99%

Advances in the study of acetaminophen-induced liver injury

Chen

2023

Front. Pharmacol.

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Acetaminophen (APAP) overdose is a significant cause of drug-induced liver injury and acute liver failure. The diagnosis, screening, and management of APAP-induced liver injury (AILI) is challenging because of the complex mechanisms involved. Starting from the current studies on the mechanisms of AILI, this review focuses on novel findings in the field of diagnosis, screening, and management of AILI. It highlights the current issues that need to be addressed. This review is supposed to summarize the recent research progress and make recommendations for future research.

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Section: Management Of Ailimentioning

confidence: 99%

Advances in the study of acetaminophen-induced liver injury

Chen

2023

Front. Pharmacol.

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“…However, it is reported that the downregulation of IL1B could be related to the anti-inflammatory response of curcumin [ 33 , 34 ]. Since the pleiotropic beneficial effects of curcumin are mainly related to its ability to act as a mediator of cellular redox balance [ 20 , 34 ], it has been listed as a natural product useful for the treatment of drug-induced liver injury or DILI [ 35 ]. However, recently, several cases of acute liver injury after consumption of curcumin as a dietary supplement have been reported [ 36 , 37 ], and it is still not clear when the hepatoprotective role switches to hepatotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Curcumin and Andrographolide Co-Administration Safely Prevent Steatosis Induction and ROS Production in HepG2 Cell Line

et al. 2023

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Non-alcoholic fatty liver disease (NAFLD) is an emerging chronic liver disease worldwide. Curcumin and andrographolide are famous for improving hepatic functions, being able to reverse oxidative stress and release pro-inflammatory cytokines, and they are implicated in hepatic stellate cell activation and in liver fibrosis development. Thus, we tested curcumin and andrographolide separately and in combination to determine their effect on triglyceride accumulation and ROS production, identifying the differential expression of genes involved in fatty liver and oxidative stress development. In vitro steatosis was induced in HepG2 cells and the protective effect of curcumin, andrographolide, and their combination was observed evaluating cell viability, lipid and triglyceride content, ROS levels, and microarray differential gene expression. Curcumin, andrographolide, and their association were effective in reducing steatosis, triglyceride content, and ROS stress, downregulating the genes involved in lipid accumulation. Moreover, the treatments were able to protect the cytotoxic effect of steatosis, promoting the expression of survival and anti-inflammatory genes. The present study showed that the association of curcumin and andrographolide could be used as a therapeutic approach to counter high lipid content and ROS levels in steatosis liver, avoiding the possible hepatotoxic effect of curcumin. Furthermore, this study improved our understanding of the antisteatosis and hepatoprotective properties of a curcumin and andrographolide combination.

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“…Researchers have found that APAP-induced liver oxidative stress and mitochondrial dysfunction are responsible for APAP-induced liver injury caused by oxidative stress and mitochondrial dysfunction 47 , 48 . APAP is believed to cause liver injury as follows: excessive intake of APAP is saturated by liver glucuronidation and sulphuration, and APAP is metabolized to form toxic NAPQI primarily by CYP4502E1, resulting in its degradation by GSH in the liver 49 , eventually causing various forms of liver cell death. Therefore, it is necessary to determine the underlying mechanism of cell death to aid in the clinical treatment of acute liver injury and liver failure caused by excessive APAP.…”

Section: Discussionmentioning

confidence: 99%

GAS1 Promotes Ferroptosis of Liver Cells in Acetaminophen-Induced Acute Liver Failure

Tao,

Xue,

Wang

et al. 2023

Int. J. Med. Sci.

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Purpose: Acute liver failure (ALF) is a clinically fatal disease that leads to the rapid loss of normal liver function. Acetaminophen (APAP) is a leading cause of drug-induced ALF. Ferroptosis, defined as iron-dependent cell death associated with lipid peroxide accumulation, has been shown to be strongly associated with APAP-induced liver injury. Growth arrest-specific 1 (GAS1) is a growth arrest-specific gene, which is closely related to the inhibition of cell growth and promotion of apoptosis. However, the functional role and underlying mechanism of GAS1 in APAP-induced ferroptosis remain unknown. Methods: We established liver-specific overexpression of GAS1 (GAS1 AAV8-OE) mice and the control (GAS1 ) mice by tail vein injection of male mice with adeno-associated virus. APAP at 500 mg/kg was intraperitoneally injected into these two groups of mice to induce acute liver failure. The shRNA packaged by the lentivirus inhibits GAS1 gene expression in human hepatoma cell line HepaRG (HepaRG-shNC and HepaRG-shGAS1-2) and primary hepatocytes of mice with liver-specific overexpression of GAS1 were isolated and induced by APAP in vitro to further investigate the regulatory role of GAS1 in APAP-induced acute liver failure. Results: APAP-induced upregulation of ferroptosis, levels of lipid peroxides and reactive oxygen species, and depletion of glutathione were effectively alleviated by the ferroptosis inhibitor, ferrostatin-1, and downregulation of GAS1 expression. GAS1 overexpression promoted ferroptosis-induced lipid peroxide accumulation via p53, inhibiting its downstream target, solute carrier family 7 member 11. Conclusion: Collectively, our findings suggest that GAS1 overexpression plays a key role in aggravating APAP-induced acute liver injury by promoting ferroptosis-induced accumulation of lipid peroxides.

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Progress in the treatment of drug-induced liver injury with natural products

Cited by 41 publications

References 175 publications

Advances in the study of acetaminophen-induced liver injury

Advances in the study of acetaminophen-induced liver injury

Curcumin and Andrographolide Co-Administration Safely Prevent Steatosis Induction and ROS Production in HepG2 Cell Line

GAS1 Promotes Ferroptosis of Liver Cells in Acetaminophen-Induced Acute Liver Failure

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