Early-life perfluorooctanoic acid exposure induces obesity in male offspring and the intervention role of chlorogenic acid

Shao, Wentao; Xu, Jin; Xu, Cheng; Weng, Zhenkun; Liu, Qian; Zhang, Xin; Liang, Jingjia; Li, Wenxiang; Zhang, Yi; Jiang, Zhaoyan; Gu, Aihua

doi:10.1016/j.envpol.2020.115974

Cited by 22 publications

(14 citation statements)

References 48 publications

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“…Total protein from frozen livers or cultured cells were extracted and used with western immunoblotting as described previously 53 . The following antibodies were used for western blot: anti-FXR (1:1000, Abcam, ab235094), anti-CYP7A1 (1:1000, Abcam, ab65596), anti-CYP8B1 (1:1000, Abcam, ab191910), anti-GAPDH (1:1000, Proteintech, 60004-1-Ig).…”

Section: Methodsmentioning

confidence: 99%

Gut microbiota promotes cholesterol gallstone formation by modulating bile acid composition and biliary cholesterol secretion

et al. 2022

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Cholesterol gallstone disease is a worldwide common disease. Cholesterol supersaturation in gallbladder bile is the prerequisite for its pathogenesis, while the mechanism is not completely understood. In this study, we find enrichment of gut microbiota (especially Desulfovibrionales) in patients with gallstone disease. Fecal transplantation of gut microbiota from gallstone patients to gallstone-resistant strain of mice can induce gallstone formation. Carrying Desulfovibrionales is associated with enhanced cecal secondary bile acids production and increase of bile acid hydrophobicity facilitating intestinal cholesterol absorption. Meanwhile, the metabolic product of Desulfovibrionales, H2S increase and is shown to induce hepatic FXR and inhibit CYP7A1 expression. Mice carrying Desulfovibrionales present induction of hepatic expression of cholesterol transporters Abcg5/g8 to promote biliary secretion of cholesterol as well. Our study demonstrates the role of gut microbiota, Desulfovibrionales, as an environmental regulator contributing to gallstone formation through its influence on bile acid and cholesterol metabolism.

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Section: Methodsmentioning

confidence: 99%

Gut microbiota promotes cholesterol gallstone formation by modulating bile acid composition and biliary cholesterol secretion

et al. 2022

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“…Total proteins from each group were extracted and detected with Western blotting as previously [ 17 ]. The antibodies were used as following: anti-CLCE2 (1:1000), anti-p-STAT1 (1:1000), anti-p-JAK1 (1:1000), anti- GAPDH (1:1000).…”

Section: Methodsmentioning

confidence: 99%

Attenuating oxidized low density lipoprotein (ox-LDL)-induced macrophages damage via inhibiting C-type lectin domain family 2 (CLEC2) expression through janus kinase 1 (JAK1)/ signal transducers and activators of transcription-1 (STAT1) pathway

2022

Bioengineered

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Our study aimed to explore the effect of C-type lectin-like receptor 2 (CLEC2) expression level on oxidized low-density lipoprotein (ox-LDL)-induced macrophage damage and the regulatory mechanism of macrophage foaming. Foam cells were derived from RAW264.7 by ox-LDL, and the cell viability was detected by cell counting kit-8 (CCK-8) assay. Enzyme-linked immunosorbent assay (ELISA) was applied to detect the levels of inflammatory cytokines tumor necrosis factor (TNF-α), Interleukin-6 (IL-6), and Interleulin-1β (IL-1β). Small interfering CLEC2 (si-CLEC2) was synthesized and transfected into RAW264.7, and the apoptosis rate was analyzed by flow cytometry. Western blotting was employed to detect the protein expressions of Janus kinase 1 (JAK1), Signal transducers and activators of transcription-1 (STAT1), phosphorylation-JAK1 (p-JAK1), phosphorylation-STAT1 (p-STAT1), CLEC2, and the apoptosis-related proteins. The levels of total cholesterol (TC) and free cholesterol (FC) were measured using colorimetric kits. Results showed that ox-LDL could activate the JAK1/STAT1 pathway of macrophages and up-regulate the expression of CLEC2. CLEC2 knockdown could reduce macrophage inflammation and lipid accumulation. Inactivating JAK1/STAT1 pathway with JAK1 inhibitor can significantly reduce the phosphorylation of STAT1 and alleviate the ox-LDL-induced damage in macrophages by regulating the expression of CLEC2. In conclusion, targeting JAK1/STAT1 to inhibit CLEC2 can attenuate ox-LDL-induced macrophage damage. This study enriched the pathogenesis of atherosclerosis and provided the possible treatment targets.

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“… [73] Perfluorooctanoic acid exposure induced model ICR mice In-vivo Attenuates obesity, disruption of gut barrier integrity, lipid metabolism disorders, and hepatic inflammation. [74] HFD induced obesity and insulin resistance model Male C57BL/6 J mice In-vivo Alters body weight gain, insulin resistance, evaluated via hyperglycemia, glucose and insulin intolerance. [75] 3 Hyperlipidemia High fat diet induced model Male Sprague-dawley rats In-vivo Represses triglycerides, acetyl-CoA carboxylase (ACC), plasma free fatty acids (FFA) and increased carnitine palmitoyltransferase-1 (CPT-1) via activation of AMPK mechanism.…”

Section: Chlorogenic Acidmentioning

confidence: 99%

Chlorogenic acid: Potential source of natural drugs for the therapeutics of fibrosis and cancer

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Lü

Zhang

et al. 2022

Translational Oncology

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Fibrosis and cancer is described by some epidemiological studies as chronic stages of different disease conditions typically characterized by uncontrolled accumulation of extra-cellular matrix (ECM), thereby leading to inflammation of tissues and organ (lungs, heart, liver and kidney) dysfunction. It is highly prevalent, and contributes to increased mortality rate worldwide. Currently, the therapeutical approaches involving selected medications (bemcentinib, pirfenidone and nintedanib) obtained synthetically, and used in clinical practices for fibrosis and cancer management and treatment has shown to be unsatisfactorily, especially during progressive stages of the disease. With regards to finding a more potent, effective, and promising curative for fibrosis and cancer, there is need for continuous experimental studies universally. However, phytochemical constituents’ particularly phenolic compounds [Chlorogenic acid (CGA)] obtained from coffee, and coffee beans have been predominantly utilized in experimental studies, due to its multiple pharmacological properties against various disease forms. Considering its natural source alongside minimal toxicity level, CGA, a major precursor of coffee have gained considerable attention nowadays from researchers worldwide, owing to its wide, efficacious and beneficial action against fibrosis and cancer. Interestingly, the safety of CGA has been proven. Furthermore, numerous experimental studies have also deduced massive remarkable outcomes in the use of CGA clinically, as a potential drug candidate against treatment of fibrosis and cancer. In the course of this review article, we systematically discussed the beneficial contributions of CGA with regards to its source, absorption, metabolism, mechanistic effects, and molecular mechanisms against different fibrosis and cancer categorization, which might be a prospective remedy in the future. Moreover, we also highlighted CGA (in vitro and in vivo analytical studies) defensive effects against various disorders.

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Early-life perfluorooctanoic acid exposure induces obesity in male offspring and the intervention role of chlorogenic acid

Cited by 22 publications

References 48 publications

Gut microbiota promotes cholesterol gallstone formation by modulating bile acid composition and biliary cholesterol secretion

Gut microbiota promotes cholesterol gallstone formation by modulating bile acid composition and biliary cholesterol secretion

Attenuating oxidized low density lipoprotein (ox-LDL)-induced macrophages damage via inhibiting C-type lectin domain family 2 (CLEC2) expression through janus kinase 1 (JAK1)/ signal transducers and activators of transcription-1 (STAT1) pathway

Chlorogenic acid: Potential source of natural drugs for the therapeutics of fibrosis and cancer

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