Leonurine alleviates acetaminophen-induced acute liver injury by regulating the PI3K/AKT signaling pathway in mice

Yan, Yu; Zhou, Shizhe; Wang, Yan; Di, Shouyi; Wang, Y; Huang, Xin; Chen, Ying

doi:10.1016/j.intimp.2023.110375

Cited by 19 publications

(9 citation statements)

References 28 publications

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“…As shown in Figure 1 , the liver weights ( Figure 1A ) and liver-to-body weight ratios ( Figure 1B ) were lower in the AD mice than in the normal mice, but no significant changes were observed after exercise. Serum AST and ALT are markers of liver injury [ 21 ], and the significant increase in serum AST and ALT in the AD mice and their significant decrease after exercise ( Figure 1C , 1D ) suggested that liver injury may have existed in the AD mice, and it was alleviated after participation in treadmill exercise. The hepatocytes of the WT mice were arranged more regularly and were clearly spaced, and the hepatic sinusoids were distributed among the hepatocytes in greater numbers and arranged in a radioactive pattern.…”

Section: Resultsmentioning

confidence: 99%

Treadmill exercise can regulate the redox balance in the livers of APP/PS1 mice and reduce LPS accumulation in their brains through the gut-liver-kupffer cell axis

Yuan,

Wang,

Yang

et al. 2024

Aging

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A growing body of clinical data has shown that patients with Alzheimer’s disease (AD) have symptoms such as liver dysfunction and microbial–gut–brain axis dysfunction in addition to brain pathology, presenting a systemic multisystemic pathogenesis. Considering the systemic benefits of exercise, here, we first observed the effects of long-term treadmill exercise on liver injuries in APP/PS1 transgenic AD mice and explored the potential mechanisms of the gut–liver–brain axis’s role in mediating exercise’s ability to reduce bacterial lipopolysaccharide (LPS) pathology in the brain. The results showed that the livers of the AD mice were in states of oxidative stress, while the mice after long-term treadmill exercise showed alleviation of their oxidative stress, their intestinal barriers were protected, and the ability of their Kupffer cells to hydrolyze LPS was improved, in addition to the accumulation of LPS in their brains being reduced. Notably, the livers of the AD mice were in immunosuppressed states, with lower pro-oxidative and antioxidative levels than the livers of the wild-type mice, while exercise increased both their oxidative and antioxidative levels. These results suggest that long-term exercise modulates hepatic redox homeostasis in AD mice, attenuates oxidative damage, and reduces the accumulation of LPS in the brain through the combined action of the intestine–liver–Kupffer cells.

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Section: Resultsmentioning

confidence: 99%

Treadmill exercise can regulate the redox balance in the livers of APP/PS1 mice and reduce LPS accumulation in their brains through the gut-liver-kupffer cell axis

Yuan,

Wang,

Yang

et al. 2024

Aging

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“…[ 59 , 60 ] Research has demonstrated that leonurine effectively alleviates DILI by modulating the PI3K/ AKT signaling pathway. [ 61 ]…”

Section: Discussionmentioning

confidence: 99%

Network pharmacology integrated with molecular docking technology to reveal the potential mechanism of Shuganfang against drug-induced liver injury

Wang,

Chen,

Wang

et al. 2023

Medicine

Self Cite

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This study aimed to investigate the active composition and mechanism of the Shuganfang (SGF) in treating drug-induced liver injury (DILI) using network pharmacology and molecular docking. The potential active ingredients and targets of SGF were obtained from the Traditional Chinese Medicine Systems Pharmacology Database (TCMSP) database. DILI-related targets were queried from various databases including GEO, GeneCards, OMIM, NCBI, and DisGeNET. The STRING database was used to establish a protein-protein interaction (PPI) network. DAVID was utilized for conducting gene ontology (GO) function enrichment and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analyses. The data visualization and analysis of herb-ingredient-target and disease-pathway-target-ingredient networks were conducted using Cytoscape software (version 3.7.2). PyMoL and AutoDock software was used to select the best binding target for molecular docking. A total of 177 active ingredients,126 targets and 10112 disease targets were obtained, including 122 intersection targets. The identified potential active ingredients consisted of quercetin, kaempferol, luteolin, tanshinone IIa, nobiletin, isorhamnetin, beta-sitosterol and naringenin. The core targets implicated in the study were IL6, estrogen receptor 1 (ESR1), hypoxia-inducible factor alpha subunit 1 (HIF1A), MYC and vascular endothelial growth factor A (VEGFA). KEGG analysis revealed that the treatment of DILI with SGF mainly acted through apoptosis, the PI3K-Akt signaling pathway, and the tumor necrosis factor (TNF) signaling pathway. Furthermore, the binding affinities between the potential ingredients and the core targets were subsequently confirmed through molecular docking experiments. The findings indicated that the docking outcomes remained consistent and demonstrated a favorable capacity for binding. SGF exerts a therapeutic effect on DILI through multiple active ingredients, multiple targets and multiple pathways. Our findings contribute to a positive investigation and establish a theoretical basis for further extensive exploration of SGF as a potential treatment for DILI in future research.

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“…PI3K/AKT1 pathway defends the myocardium by suppressing or strengthening the expression of downstream related target proteins. AKT1 is activated by activating PI3K, and then apoptosis is mediated by regulating Bcl-2 factor (Yu et al, 2023). Sun proposed that Bcl-2 family proteins regulate ISO-induced cardiac apoptosis by down-regulating Bcl-2 and up-regulating Bax (Sun et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Magnesium isoglycyrrhizinate regulates oxidative stress and apoptosis via PI3K/AKT1 pathway to improve myocardial remodeling in mice

Qian,

Zhou,

et al. 2023

Preprint

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The role of magnesium isoglycyrrhizinate (MgIG) in myocardial remodeling is being investigated. We evaluated the result of MgIG on isoproterenol (ISO) -enticed myocardial remodeling in mice by activating the PI3K/AKT1 pathway. The heart function of mice was tested by echocardiography, and it was found that MgIG could improve the left ventricular function. Pathological staining analysis showed that MgIG could decrease the degree of myocardial injury caused by ISO. The serum data detected by ELISA showed that MgIG could reduce the content of CK-MB, MDA and LDH, and increase the activity of GSH-Px. Western blotting showed that the protein expressions of Collagen Ⅰ, BNP, Bax, Cleaved caspase-3, p-PI3K and p-AKT1 were decreased, while the protein expressions of Bcl-2, COX2 and SOD1 were increased. Meanwhile activation of the PI3K activator (740Y-P) reverses the cardioprotective effect of MgIG. These findings suggest that the myocardial remodeling induced by ISO could be improved by MgIG, and its mechanism may be associated with inhibite PI3K/AKT1 pathway to regulate apoptosis and oxidative stress.

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Leonurine alleviates acetaminophen-induced acute liver injury by regulating the PI3K/AKT signaling pathway in mice

Cited by 19 publications

References 28 publications

Treadmill exercise can regulate the redox balance in the livers of APP/PS1 mice and reduce LPS accumulation in their brains through the gut-liver-kupffer cell axis

Treadmill exercise can regulate the redox balance in the livers of APP/PS1 mice and reduce LPS accumulation in their brains through the gut-liver-kupffer cell axis

Network pharmacology integrated with molecular docking technology to reveal the potential mechanism of Shuganfang against drug-induced liver injury

Magnesium isoglycyrrhizinate regulates oxidative stress and apoptosis via PI3K/AKT1 pathway to improve myocardial remodeling in mice

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