Protective effects of resveratrol against fumonisin B1-induced liver toxicity in mice

Yalcin, Rıza; Kart, Asim; Özmen, Özlem; ZEYBEK, Esra

doi:10.2478/aiht-2023-74-3648

Cited by 2 publications

(2 citation statements)

References 29 publications

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“…At the end of the experiment, we firstly analyzed whether acacetin showed potential toxicities in animals. Serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) have been used as major biomarkers for liver damage, especially as biomarkers for substances-induced liver toxicity 17 , 18 . We found that 10 mg/kg acacetin showed no effect, while 20 mg/kg acacetin significantly reduced the serum levels of ALT and AST (Supplementary Fig.…”

Section: Resultsmentioning

confidence: 99%

Acacetin inhibited non-small-cell lung cancer (NSCLC) cell growth via upregulating miR-34a in vitro and in vivo

Li,

Zhong,

Zhao

et al. 2024

Sci Rep

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Acacetin, one of the flavonoid compounds, is a natural product found in various plants, including Silver birch, and Damiana. Previous studies showed that acacetin has anti-cancer effects on many kinds of cancer cells, however, the role of and the mechanisms of actions of acacetin on non-small cell lung cancer (NSCLC) cells is still not fully understood. Herein, we found that, in vitro, acacetin inhibited the proliferation, invasion, and migration of NSCLC cells, A549 and H460, in a dose-dependent manner. Meanwhile, flow cytometry assay results showed that acacetin induced G2/M phase cell cycle arrest, and apoptosis of NSCLC cells. In vivo, acacetin suppressed tumor formation of A549-xenografted nude mice model with no obvious toxicities. Western blotting results showed that the protein levels of cell cycle-related proteins cyclin B1, cyclin D, and anti-apoptotic protein Bcl-2 had decreased, while the apoptosis-related protein Bak had increased both in NSCLC cells and in A549-xenografted tumor tissues. For investigating the molecular mechanism behind the biological effects of acacetin on NSCLC, we found that acacetin induced the expression levels of tumor suppressor p53 both in vitro and in vivo. MicroRNA, miR-34a, the direct target of p53, has been shown anti-NSCLC proliferation effects by suppressing the expression of its target gene programmed death ligand 1 (PD-L1). We found that acacetin upregulated the expression levels of miR-34a, and downregulated the expression levels of PD-L1 of NSCLC cells in vitro and of tumors in vivo. In vitro, knockdown p53 expression by siRNAs reversed the induction effects of acacetin on miR34a expression and abolished the inhibitory activity of acacetin on NSCLC cell proliferation. Furthermore, using agomir and antagomir to overexpress and suppress the expression miR-34a in NSCLC cells was also examined. We found that miR-34a agomir showed similar effects as acacetin on A549 cells, while miR-34a antagomir could partially or completely reverse acacetin’s effects on A549 cells. In vivo, intratumor injection of miR-34a antagomir could drastically suppress the anti-tumor formation effects of acacetin in A549-xenografted nude mice. Overall, our results showed that acacetin inhibits cell proliferation and induces cell apoptosis of NSCLC cells by regulating miR-34a.

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Section: Resultsmentioning

confidence: 99%

Acacetin inhibited non-small-cell lung cancer (NSCLC) cell growth via upregulating miR-34a in vitro and in vivo

Li,

Zhong,

Zhao

et al. 2024

Sci Rep

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“…This toxicity also becomes much more pronounced with increased adiposity ( 89 ). Nevertheless, a recent study showed that these adverse effects can be mitigated when resveratrol is co-administered, as this polyphenol acts as an hepato-protector ( 90 ).…”

Section: Experimental/clinical Evidence Of Therapies Targeting Sphing...mentioning

confidence: 99%

Therapeutic implications for sphingolipid metabolism in metabolic dysfunction-associated steatohepatitis

Ramos-Molina,

Rossell,

Pérez-Montes de Oca

et al. 2024

Front. Endocrinol.

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The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD), a leading cause of chronic liver disease, has increased worldwide along with the epidemics of obesity and related dysmetabolic conditions characterized by impaired glucose metabolism and insulin signaling, such as type 2 diabetes mellitus (T2D). MASLD can be defined as an excessive accumulation of lipid droplets in hepatocytes that occurs when the hepatic lipid metabolism is totally surpassed. This metabolic lipid inflexibility constitutes a central node in the pathogenesis of MASLD and is frequently linked to the overproduction of lipotoxic species, increased cellular stress, and mitochondrial dysfunction. A compelling body of evidence suggests that the accumulation of lipid species derived from sphingolipid metabolism, such as ceramides, contributes significantly to the structural and functional tissue damage observed in more severe grades of MASLD by triggering inflammatory and fibrogenic mechanisms. In this context, MASLD can further progress to metabolic dysfunction-associated steatohepatitis (MASH), which represents the advanced form of MASLD, and hepatic fibrosis. In this review, we discuss the role of sphingolipid species as drivers of MASH and the mechanisms involved in the disease. In addition, given the absence of approved therapies and the limited options for treating MASH, we discuss the feasibility of therapeutic strategies to protect against MASH and other severe manifestations by modulating sphingolipid metabolism.

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Protective effects of resveratrol against fumonisin B1-induced liver toxicity in mice

Cited by 2 publications

References 29 publications

Acacetin inhibited non-small-cell lung cancer (NSCLC) cell growth via upregulating miR-34a in vitro and in vivo

Acacetin inhibited non-small-cell lung cancer (NSCLC) cell growth via upregulating miR-34a in vitro and in vivo

Therapeutic implications for sphingolipid metabolism in metabolic dysfunction-associated steatohepatitis

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