4-Hydroxyderricin Promotes Apoptosis and Cell Cycle Arrest through Regulating PI3K/AKT/mTOR Pathway in Hepatocellular Cells

Gao, Xiang; Jiang, Yulin; Xu, Qi; Liu, Feng; Pang, Xuening; Wang, Mingji; Li, Qun; Li, Zichao

doi:10.3390/foods10092036

Cited by 11 publications

(10 citation statements)

References 60 publications

(58 reference statements)

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“…In this study, Fn041 and LGG reduced high-fat diet-induced lipid accumulations in the adipose tissues of the epididymis and liver, which may at least partially explain their weight loss efficacy. This is consistent with the results of a previous intervention study that demonstrated that Fn041 exerts an inhibitory effect on high-fat diet-induced hepatic steatosis by downregulating Fas mRNA expression and upregulating Srebp1c mRNA expression ( 17 , 33 ). LGG has also prevented liver steatosis and adipocyte enlargement caused by a high-fat diet ( 34 ).…”

Section: Discussionsupporting

confidence: 92%

Prevention of High-Fat Diet-Induced Hypercholesterolemia by Lactobacillus reuteri Fn041 Through Promoting Cholesterol and Bile Salt Excretion and Intestinal Mucosal Barrier Functions

Sun

Zhao

et al. 2022

Front. Nutr.

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Objectives:Lactobacillus reuteri Fn041 (Fn041) is a probiotic isolated from immunoglobulin A coated microbiota in the human breast milk of Gannan in China with a low incidence of hypercholesterolemia. This study aims to explore the role and mechanism of Fn041 in preventing hypercholesterolemia caused by a high-fat diet in mice.MethodsC57BL/6N mice were fed a low-fat diet or a high-fat diet and gavage with Fn041 and Lactobacillus rhamnosus GG (LGG) for 8 weeks.ResultsBoth Fn041 and LGG prevented the occurrence of hypercholesterolemia, liver and testicular fat accumulation. In addition, a high-fat diet causes intestinal dysbiosis and mucosal barrier damage, which is associated with hypercholesterolemia. Fn041 prevented the high-fat diet-induced reduction in alpha diversity of intestinal microbiota and intestinal mucosal barrier damage. Fn041 treatment significantly increased fecal total cholesterol and total bile acids.ConclusionsFn041 prevented hypercholesterolemia by enhancing cholesterol excretion and mucosal barrier function.

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Section: Discussionsupporting

confidence: 92%

Prevention of High-Fat Diet-Induced Hypercholesterolemia by Lactobacillus reuteri Fn041 Through Promoting Cholesterol and Bile Salt Excretion and Intestinal Mucosal Barrier Functions

Sun

Zhao

et al. 2022

Front. Nutr.

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“…Studies have revealed that autophagy mainly consists of the PI3K/Akt/mTOR pathway and the Beclin 1 pathway, which is a key regulation protein of autophagy [ 34 ]. The mTOR signaling pathway is a critical regulation of autophagy initiation, activated mTOR inhibits autophagy [ 35 ]. After acrolein treatment, the expression of Beclin 1 increased, and the p-mTOR and p-akt content significantly decreased.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Ganoderma atrum Polysaccharide on Acrolein-Induced Apoptosis and Autophagic Flux in IEC-6 Cells

Wang¹,

Chang²,

Zheng³

et al. 2022

Foods

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This study was designed to explore the beneficial effect and mechanism of Ganoderma atrum (G. atrum) polysaccharide (PSG-1) on acrolein-induced IEC-6 cells. Our results indicated that PSG-1 significantly reduced the impairment of acrolein on cell viability, decreased oxidative stress, and enabled normal expression of tight junction (TJ) proteins that were inhibited by acrolein in IEC-6 cells. Furthermore, PSG-1 attenuated the elevation of microtubule-associated proteins light chain 3 (LC3) and Beclin 1-like protein 1 (Beclin 1) and increased the protein levels of phospho-mTOR (p-mTOR) and phospho-akt (p-akt), indicating that PSG-1 activated the mammalian target of rapamycin (mTOR) signaling pathway and alleviated acrolein-induced autophagy in IEC-6 cells. Moreover, PSG-1 markedly attenuated the acrolein-induced apoptosis, as evidenced by the increase in mitochondrial membrane potential (MMP) and B-cell lymphoma 2 (Bcl-2) expression, and the decrease in cysteine aspartate lyase (caspase)-3 and caspase-9. In addition, autophagy the inhibitor inhibited acrolein-induced TJ and apoptosis of IEC-6 cells, while the apoptosis inhibitor also inhibited acrolein-induced TJ and autophagy, suggesting that autophagy and apoptosis were mutually regulated. Taken together, the present study proved that PSG-1 could protect IEC-6 cells from acrolein-induced oxidative stress and could repair TJ by inhibiting apoptosis and autophagic flux, where autophagy and apoptosis were mutually regulated.

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“…Demethyleneberberine caused G1 arrest of lung cancer cells by down-regulating c-Myc/HIF1A [ 467 ]. 4-Hydroxyderricin, an Angelica keiskei Koidzumi-derived natural product, induced G1 or G2/M arrest for liver cancer cells (HepG2 and Huh7 cells) by down-regulating mTOR [ 473 ]. Bufadienolide, a traditional Chinese drug Chan’Su-derived cardiac glycoside, caused G1 arrest of breast and prostate cancer cells by inhibiting insulin-like growth factor-I (IGF1)-activated phosphorylation of mTOR, S6K1, and 4EBP1 [ 476 ].…”

Section: Natural Products Regulate Akt Effectors-modulated Cell Funct...mentioning

confidence: 99%

The Impact of Oxidative Stress and AKT Pathway on Cancer Cell Functions and Its Application to Natural Products

et al. 2022

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Oxidative stress and AKT serine-threonine kinase (AKT) are responsible for regulating several cell functions of cancer cells. Several natural products modulate both oxidative stress and AKT for anticancer effects. However, the impact of natural product-modulating oxidative stress and AKT on cell functions lacks systemic understanding. Notably, the contribution of regulating cell functions by AKT downstream effectors is not yet well integrated. This review explores the role of oxidative stress and AKT pathway (AKT/AKT effectors) on ten cell functions, including apoptosis, autophagy, endoplasmic reticulum stress, mitochondrial morphogenesis, ferroptosis, necroptosis, DNA damage response, senescence, migration, and cell-cycle progression. The impact of oxidative stress and AKT are connected to these cell functions through cell function mediators. Moreover, the AKT effectors related to cell functions are integrated. Based on this rationale, natural products with the modulating abilities for oxidative stress and AKT pathway exhibit the potential to regulate these cell functions, but some were rarely reported, particularly for AKT effectors. This review sheds light on understanding the roles of oxidative stress and AKT pathway in regulating cell functions, providing future directions for natural products in cancer treatment.

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4-Hydroxyderricin Promotes Apoptosis and Cell Cycle Arrest through Regulating PI3K/AKT/mTOR Pathway in Hepatocellular Cells

Cited by 11 publications

References 60 publications

Prevention of High-Fat Diet-Induced Hypercholesterolemia by Lactobacillus reuteri Fn041 Through Promoting Cholesterol and Bile Salt Excretion and Intestinal Mucosal Barrier Functions

Prevention of High-Fat Diet-Induced Hypercholesterolemia by Lactobacillus reuteri Fn041 Through Promoting Cholesterol and Bile Salt Excretion and Intestinal Mucosal Barrier Functions

Protective Effect of Ganoderma atrum Polysaccharide on Acrolein-Induced Apoptosis and Autophagic Flux in IEC-6 Cells

The Impact of Oxidative Stress and AKT Pathway on Cancer Cell Functions and Its Application to Natural Products

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