MiR-27a-5p regulates acrylamide-induced mitochondrial dysfunction and intrinsic apoptosis via targeting Btf3 in rats

Zhang, Lujia; Li, Dong; Yang, Liuqing; Luo, Yinghua; Chen, Fang

doi:10.1016/j.foodchem.2021.130816

Cited by 19 publications

(23 citation statements)

References 41 publications

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“…Mitochondria are key organelles in which aerobic respiration produces energy, and they play a vital role in cellular physiology. Furthermore, changes to the MMP are used as an important indicator to evaluate the mitochondrial function in cells . Normally, the MMP is in a state of dynamic equilibrium in which ions cross the membrane to support the function of the mitochondria.…”

Section: Resultsmentioning

confidence: 99%

“…Furthermore, changes to the MMP are used as an important indicator to evaluate the mitochondrial function in cells. 23 Normally, the MMP is in a state of dynamic equilibrium in which ions cross the membrane to support the function of the mitochondria. When the mitochondrial function is adversely affected, the production of ATP is directly affected, 24 impairing the physiological role of the mitochondrial respiratory chain.…”

Section: ■ Resultsmentioning

confidence: 99%

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Natural Compound 2-Chloro-1,3-dimethoxy-5-methylbenzene, Isolated from Hericium Erinaceus, Inhibits Fungal Growth by Disrupting Membranes and Triggering Apoptosis

Qian

Zhang

Wang

et al. 2022

J. Agric. Food Chem.

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In this study, 2-chloro-1,3-dimethoxy-5-methylbenzene (CDM), a natural product with anti-Candida albicans activity, was discovered from the Hericium erinaceus mycelium. The minimum inhibitory concentration of CDM was 62.5 μg/mL. Moreover, structural analogues of CDM obtained from chemical synthesis were applied to explore the structure−activity relationship (SAR) of CDM against C. albicans. It was found that methoxy groups, halogen atoms (except fluorine atoms), and methoxy-meta-position methyl groups in the structure of CDM were the key active groups. Furthermore, we investigated the anti-C. albicans mechanism of CDM. Experiments suggested that CDM destroyed the cell membrane of C. albicans, including the cytoplasmic membrane and mitochondrial membrane, and caused the accumulation of reactive oxygen species and mitochondrial dysfunction, which ultimately led to apoptosis of C. albicans. In addition, CDM had no toxicity on human normal gastric mucosal epithelial cells exposed to a concentration of 125 μg/mL. Experiments showed that CDM reduced the damage of C. albicans to the visceral tissue of infected mice and improved the survival rate of mice. Our research provides a scientific basis for the discovery of effective and safe anti-C. albicans drugs from H. erinaceus.

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Section: Resultsmentioning

confidence: 99%

Section: ■ Resultsmentioning

confidence: 99%

Natural Compound 2-Chloro-1,3-dimethoxy-5-methylbenzene, Isolated from Hericium Erinaceus, Inhibits Fungal Growth by Disrupting Membranes and Triggering Apoptosis

Qian

Zhang

Wang

et al. 2022

J. Agric. Food Chem.

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“…The changes in mitochondrial membrane potential (Δψm) were observed with JC-1 staining dye assay kit (Beijing Solarbio Science & Technology Co., Ltd., Beijing, China), according to the method described by early literature [ 86 ]. JC-1 dye is a lipophilic cationic fluorescent dye with dual (red and green) emission wavelengths, and the attenuation of its red/green fluorescence intensity ratio is commonly used to represent an increase in mitochondrial membrane depolarization.…”

Section: Methodsmentioning

confidence: 99%

Quercetin Reprograms Immunometabolism of Macrophages via the SIRT1/PGC-1α Signaling Pathway to Ameliorate Lipopolysaccharide-Induced Oxidative Damage

Peng

Yang

et al. 2023

IJMS

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The redox system is closely related to changes in cellular metabolism. Regulating immune cell metabolism and preventing abnormal activation by adding antioxidants may become an effective treatment for oxidative stress and inflammation-related diseases. Quercetin is a naturally sourced flavonoid with anti-inflammatory and antioxidant activities. However, whether quercetin can inhibit LPS-induced oxidative stress in inflammatory macrophages by affecting immunometabolism has been rarely reported. Therefore, the present study combined cell biology and molecular biology methods to investigate the antioxidant effect and mechanism of quercetin in LPS-induced inflammatory macrophages at the RNA and protein levels. Firstly, quercetin was found to attenuate the effect of LPS on macrophage proliferation and reduce LPS-induced cell proliferation and pseudopodia formation by inhibiting cell differentiation, as measured by cell activity and proliferation. Subsequently, through the detection of intracellular reactive oxygen species (ROS) levels, mRNA expression of pro-inflammatory factors and antioxidant enzyme activity, it was found that quercetin can improve the antioxidant enzyme activity of inflammatory macrophages and inhibit their ROS production and overexpression of inflammatory factors. In addition, the results of mitochondrial morphology and mitochondrial function assays showed that quercetin could upregulate the mitochondrial membrane potential, ATP production and ATP synthase content decrease induced by LPS, and reverse the mitochondrial morphology damage to a certain extent. Finally, Western blotting analysis demonstrated that quercetin significantly upregulated the protein expressions of SIRT1 and PGC-1α, that were inhibited by LPS. And the inhibitory effects of quercetin on LPS-induced ROS production in macrophages and the protective effects on mitochondrial morphology and membrane potential were significantly decreased by the addition of SIRT1 inhibitors. These results suggested that quercetin reprograms the mitochondria metabolism of macrophages through the SIRT1/PGC-1α signaling pathway, thereby exerting its effect of alleviating LPS-induced oxidative stress damage.

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“…Studies have shown that AA induces hepatocyte apoptosis, leading to an increase of bax, TGF-β1, and COX-2 and decreases the expression of bcl-2, Nrf2, HO-1, and antioxidant [88]. AA also stimulated apoptosis in HepG2 cell, rat liver cells (e.g., BRL-3A cells and IAR20 cells), and kidney cells, and the miR-27a-5p-Btf3-ATM-p53 axis might play a vital role in the promotion of AA-induced cell apoptosis through disrupting mitochondrial structure and function [89]. It was reported that the application of AA increased the level of KIM-1 in kidney tissue, as well as the expression levels of caspase-3 and bcl-2.…”

Section: Acrylamide Induces Apoptosis In Liver Kidney and Lungmentioning

confidence: 96%

Research Progress of Programmed Cell Death Induced by Acrylamide

Wang

et al. 2023

Journal of Food Quality

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Acrylamide exposure through environment pollution and diet is very common in daily life. With the deepening of the study on the toxicity of acrylamide, it has attracted widespread attention for the effects of acrylamide on multiple organs through affecting a variety of programmed cell death. Multiple studies have shown that acrylamide could exert its toxic effect by inducing programmed cell death, but its specific molecular mechanism is still unclear. In this review, the research on the main forms of programmed cell death (apoptosis, autophagy, and programmed necrosis) induced by acrylamide and their possible mechanisms are reviewed. This review may provide basic data for further research of acrylamide and prevention of its toxicity.

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MiR-27a-5p regulates acrylamide-induced mitochondrial dysfunction and intrinsic apoptosis via targeting Btf3 in rats

Cited by 19 publications

References 41 publications

Natural Compound 2-Chloro-1,3-dimethoxy-5-methylbenzene, Isolated from Hericium Erinaceus, Inhibits Fungal Growth by Disrupting Membranes and Triggering Apoptosis

Natural Compound 2-Chloro-1,3-dimethoxy-5-methylbenzene, Isolated from Hericium Erinaceus, Inhibits Fungal Growth by Disrupting Membranes and Triggering Apoptosis

Quercetin Reprograms Immunometabolism of Macrophages via the SIRT1/PGC-1α Signaling Pathway to Ameliorate Lipopolysaccharide-Induced Oxidative Damage

Research Progress of Programmed Cell Death Induced by Acrylamide

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