Chlorogenic acid prevents hepatotoxicity in arsenic-treated mice: role of oxidative stress and apoptosis

Dkhil, Mohamed A.; Moneim, Ahmed E. Abdel; Bauomy, Amira A.; Khalil, M.; Al-Shaebi, Esam M.; Al‐Quraishy, Saleh

doi:10.1007/s11033-019-05217-4

Cited by 59 publications

(32 citation statements)

References 37 publications

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“…The obtained results of high hepatic NO levels suggested that Pb can induce oxidative stress by the induction of reactive nitrogen species (RNS) formation; this is in agreement with the results of other studies [47,50]. Excess NO reacts with the superoxide anion (O 2 ) and forms the peroxynitrite (ONOO − ) radical, which is a potent biological oxidant and much more reactive than its parent compounds, NO and O 2 − • [51].…”

Section: Discussionsupporting

confidence: 89%

Antagonistic Efficacy of Luteolin against Lead Acetate Exposure-Associated with Hepatotoxicity is Mediated via Antioxidant, Anti-Inflammatory, and Anti-Apoptotic Activities

et al. 2019

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The abundant use of lead (Pb; toxic heavy metal) worldwide has increased occupational and ecosystem exposure, with subsequent negative health effects. The flavonoid luteolin (LUT) found in many natural foodstuffs possesses antioxidant and anti-inflammatory properties. Herein, we hypothesized that LUT could mitigate liver damage induced by exposure to lead acetate (PbAc). Male Wistar rats were allocated to four groups: control group received normal saline, LUT-treated group (50 mg/kg, oral, daily), PbAc-treated group (20 mg/kg, i.p., daily), and LUT+PbAc-treated group (received the aforementioned doses via the respective routes of administration); the rats were treated for 7 days. The results revealed that PbAc exposure significantly increased hepatic Pb residue and serum activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin value. Oxidative reactions were observed in the liver tissue following PbAc intoxication, characterized by the depletion and downregulation of antioxidant proteins (glutathione, glutathione reductase, glutathione peroxidase, superoxide dismutase, catalase, nuclear factor erythroid 2-related factor 2, and heme oxygenase-1), and an increase in oxidants (malondialdehyde and nitric oxide). Additionally, PbAc increased the release and expression of the pro-inflammatory cytokines (tumor necrosis factor alpha and interleukin-1 beta), inducible nitric oxide synthase, and nuclear factor kappa B. Moreover, PbAc enhanced hepatocyte loss by increasing the expression of pro-apoptotic proteins (Bax and caspase-3) and downregulating the anti-apoptotic protein (Bcl-2). The changes in the aforementioned parameters were further confirmed by noticeable histopathological lesions. LUT supplementation significantly reversed all of the tested parameters in comparison with the PbAc-exposed group. In conclusion, our findings describe the potential mechanisms involved in the alleviation of PbAc-induced liver injury by luteolin via its potent anti-inflammatory, antioxidant, and anti-apoptotic properties.

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Section: Discussionsupporting

confidence: 89%

Antagonistic Efficacy of Luteolin against Lead Acetate Exposure-Associated with Hepatotoxicity is Mediated via Antioxidant, Anti-Inflammatory, and Anti-Apoptotic Activities

et al. 2019

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“…Consistently, CGA alleviates renal injury by reducing inflammation and inducing epithelial cells proliferation (Arfian et al, 2019). CGA abrogates the upregulation of TNF-α and IL-1β and histological changes induced by NaAsO treatment (Dkhil et al, 2020). Taken together, CGA treatment can alleviate ST infection in vivo and in vitro.…”

Section: Discussionmentioning

confidence: 80%

Chlorogenic Acid Promotes Autophagy and Alleviates Salmonella Typhimurium Infection Through the lncRNAGAS5/miR-23a/PTEN Axis and the p38 MAPK Pathway

Tan

Fang

et al. 2020

Front. Cell Dev. Biol.

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Background: Salmonella typhimurium (ST) causes several intestinal diseases. Polyphenols including chlorogenic acid (CGA) inhibit pathogenesis. Objective: This study aimed to investigate the mechanisms of CGA in ST infection. Methods: The intestinal pathological changes and survival rate of ST-infected mice were measured to verify the protection of CGA on ST infection. The antibacterial effects of CGA in vitro on the invasion to intestinal epithelial cells and autophagy was evaluated. The relationships among GAS5, miR-23a, and PTEN were verified. Expression of inflammation-and autophagy-related proteins was detected. Results: CGA treatment alleviated pathological damage, improved the secretion disturbance of intestinal cytokines caused by ST infection, and reduced the mortality of mice. Intestinal GAS5 was upregulated after CGA treatment. LncRNA GAS5 competitively bound to miR-23a to upregulate PTEN and inhibit the p38 MAPK pathway. CGA regulated the p38 MAPK pathway through lncRNA GAS5/miR-23a/PTEN axis to promote autophagy in ST infection. The functional rescue experiments of miR-23a and PTEN further identified these effects. Conclusion: CGA promotes autophagy and inhibits ST infection through the GAS5/miR-23a/PTEN axis and the p38 MAPK pathway.

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“…Our findings are in agreement with those reported by Ye et al 31 who demonstrated the excellent antioxidant effects of CGA against streptozotocin-induced diabetic nephropathy in rats. Moreover, Dkhil et al 4 have reported that CGA improves weight loss in animals and restores the body and liver weight to normal levels. The findings of Lafay et al 11 and Bagdas et al 13 regarding phenolic compounds (such as CGA) having potential roles in regulating nutrient (e.g., protein and lipid) metabolism in liver tissues may explain the improvements in the bwt of animals following the combined exposure to CGA and arsenite.…”

Section: Discussionmentioning

confidence: 99%

“…3 Global estimates suggest that 200 million individuals are affected by As intoxication through contaminated food and water, and occupational exposure. 4 Acute As poisoning induces multiorgan failure and thus is fatal. In particular, chronic As poisoning leads to different types of cancer and organ toxicity in various organs, including the kidney, liver, and testis, and is associated with chronic immunotoxicity.…”

Section: Introductionmentioning

confidence: 99%

“…14 Furthermore, other studies have suggested the protective effects of CGA against neurotoxicity, hepatotoxicity, and cardiotoxicity. 4,[15][16][17] The present study aimed to investigate the protective effect of CGA against As-induced renal toxicity in mice through its antioxidant, anti-inflammatory and antiapoptotic activity. To the best of our knowledge, there is no data on the protective effect of CGA against As-mediated nephrotoxicity in mice, and this study is the first to report such findings.…”

Section: Introductionmentioning

confidence: 99%

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Nephroprotective effects of chlorogenic acid against sodium arsenite‐induced oxidative stress, inflammation, and apoptosis

et al. 2020

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BACKGROUND: Chronic exposure to arsenic (As) leads to serious renal disorders. Chlorogenic acid (CGA), a phenolic compound, has several well known physiological benefits, including antioxidant and anti-inflammatory activities. The present study investigated the potential renoprotective effects of CGA on sodium arsenite (NaAsO 2)-induced kidney damage in mice. The mice were randomly allocated into five groups to receive daily treatment with CGA (200 mg kg −1), NaAsO 2 (5 mg kg −1), NaAsO 2 + CGA (100 mg kg −1), NaAsO 2 + CGA (200 mg kg −1), or a control for 28 days. RESULTS: In the NaAsO 2-treated group, NaAsO 2 induced significant renal dysfunction, oxidative damage, inflammation, and apoptosis, as demonstrated by marked increases in urea and creatinine levels accompanied by a decrease in the kidney index. Considerable increases in malondialdehyde and nitric oxide levels and parallel decreases in various antioxidant markers (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione) levels were also detected in the renal tissues of NaAsO 2-treated mice. NaAsO 2 exposure was associated with marked increases in renal inflammatory markers (interleukin-1⊎ and tumor necrosis factor-⊍) and apoptosis indicators including Bax and caspase-3 levels contaminant, with a marked decrease in Bcl-2, an anti-apoptotic protein, in the NaAsO 2-treated group compared with the control group. However, pretreatment with CGA substantially mitigated the renal injury and dysfunction associated with NaAsO 2 exposure by reducing tissue inflammation and apoptosis and improving the antioxidant status. The CGA pretreatment also alleviated the NaAsO 2induced histological alterations in renal tissues. CONCLUSION: Taken together, our results suggest the efficacy of CGA in alleviating As-mediated renal tissue damage.

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Chlorogenic acid prevents hepatotoxicity in arsenic-treated mice: role of oxidative stress and apoptosis

Cited by 59 publications

References 37 publications

Antagonistic Efficacy of Luteolin against Lead Acetate Exposure-Associated with Hepatotoxicity is Mediated via Antioxidant, Anti-Inflammatory, and Anti-Apoptotic Activities

Antagonistic Efficacy of Luteolin against Lead Acetate Exposure-Associated with Hepatotoxicity is Mediated via Antioxidant, Anti-Inflammatory, and Anti-Apoptotic Activities

Chlorogenic Acid Promotes Autophagy and Alleviates Salmonella Typhimurium Infection Through the lncRNAGAS5/miR-23a/PTEN Axis and the p38 MAPK Pathway

Nephroprotective effects of chlorogenic acid against sodium arsenite‐induced oxidative stress, inflammation, and apoptosis

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