Hepatoprotective, antioxidant and, anti-inflammatory potentials of gallic acid in carbon tetrachloride-induced hepatic damage in Wistar rats

Ojeaburu, Sam I.; Oriakhi, Kelly

doi:10.1016/j.toxrep.2021.01.001

Cited by 58 publications

(33 citation statements)

References 42 publications

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“…These ndings suggested appreciable antioxidant and anti-in ammatory activity which serves as a hepatoprotective and hypocholesterolemic ingredients (Das et al 2021). As natural antioxidants, catechins can be ameliorated liver diseases by overcome the load of in ammation (Ojeaburu et al 2021).…”

Section: Discussionmentioning

confidence: 99%

Polyphenols from Green tea revert CCl4-Induced liver oxidative stress and inflammation associated with high fat diet by activation of NRF-2 and TIMP-1 pathways to neutralize ROS

Kanwal

Majeed

Awan

et al. 2022

Preprint

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Hepatic disorders are progressed by oxidative stress, chronic inflammation, hepatocyte death and increased transforming growth factor. Herein we investigated the phytochemical screening of green tea (Camellia sinensis) and analyzed its anti-oxidant and anti-inflammatory potential on liver biomarkers that elaborate therapeutic efficacy of polyphenols (catechins) in rat model associated with CCl4 induced liver injury along high fat diet. Pro-inflammatory cytokines are stimulated by either acute or chronic liver injury and critically triggered the production of inflammation, steatosis, fibrosis and liver carcinoma. We designed HPLC work to isolate the green tea phytochemical constituents quantitatively in a remarkable therapeutic range. Anti-inflammatory and antioxidant activities were carried out in vivo using treatment with green tea polyphenol extract (GTPE 600 mg/kg) that significantly reduced (P < 0,001) pro-inflammatory cytokines like tumor necrosis factor α (TNF α) and interleukin 6 (IL-6) in CCl4-induced hepatic injury in Wistar albino rats. Hepatoprotective potential of GTPE was evaluated through biochemical parameters (complete blood count, liver functional tests and lipid profile), oxidative stress biomarkers (MDA, CAT, GPx and SOD) as well as histopathological analysis. Study of NRF-2 and TIMP-1 pathways through qRT-PCR provided strategy to delay the progression of liver injury into liver fibrosis by neutralizing reactive oxygen species and reverting inflammatory cytokines with the help of GTPE in therapeutic dose. Pharmacological confirmation of current study indicated that green tea possessed incredible anti-oxidative and anti-inflammatory properties, suggesting that polyphenols providing active components (catechins) of crude extract.

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Section: Discussionmentioning

confidence: 99%

Polyphenols from Green tea revert CCl4-Induced liver oxidative stress and inflammation associated with high fat diet by activation of NRF-2 and TIMP-1 pathways to neutralize ROS

Kanwal

Majeed

Awan

et al. 2022

Preprint

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“…To measure the concentration of thiol groups, the researchers used Zantox kits (Birjand, Iran) and the Ellman's reagent (5.5′-dithiobis-(2-nitrobenzoic acid) or DTNB) [ 32 ]. Briefly, 200 μL of reaction buffer was added to 10 μL of the samples and standard solutions.…”

Section: Methodsmentioning

confidence: 99%

Effect of tannic acid-templated mesoporous silica nanoparticles on iron-induced oxidative stress and liver toxicity in rats

et al. 2021

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“…Prolonged exposure to CCl 4 can promote lipid peroxidation, and reactive oxygen species (ROS) are excessively produced in the body, leading to the consumption of glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), and myeloperoxidase (MPO) formation, which causes oxidative stress [ 7 ]. The induction of CCl 4 further lures inflammation in the liver tissues, leading to the release of various inflammatory cytokines, such as tumor necrosis factor-alpha (TNF- α , IL-6, and IL-1 β ), and inflammatory regulators (Cox2 and iNOS), thus causing hepatitis [ 8 ]. Moreover, the increase of inflammatory cytokines leads to further aggravation in the oxidative stress, thereby maintaining a vicious circle, leading to the conversion of HSCs from a resting state to myofibroblast-like cells, then activating the myofibroblasts, which are responsible for matrix remodeling and the increasing levels of ECM proteins such as collagen, desmin, vimentin, and laminin [ 9 ], thereby leading to liver fibrosis, liver cirrhosis, and liver cancer.…”

Section: Introductionmentioning

confidence: 99%

Huangjia Ruangan Granule Inhibits Inflammation in a Rat Model with Liver Fibrosis by Regulating TNF/MAPK and NF-κB Signaling Pathways

Cai

Wang²,

Zhang

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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The Huangjia Ruangan granule (HJRG) is a clinically effective Kampo formula, which has a significant effect on liver fibrosis and early liver cirrhosis. However, the mechanism underlying HJRG in treating liver fibrosis remains unclear. In this study, carbon tetrachloride (CCl4) was used to induce liver fibrosis in rats to clarify the effect of HJRG on liver fibrosis and its mechanism. Using network pharmacology, the potential mechanism of HJRG was initially explored, and a variety of analyses were performed to verify this mechanism. In the liver fibrosis model, treatment with HJRG can maintain the liver morphology, lower the levels of AST and ALT in the serum, and ameliorate pathological damage. Histopathological examinations revealed that the liver structure was significantly improved and fibrotic changes were alleviated. It can effectively inhibit collagen deposition and the expression of α-SMA, reduce the levels of the rat serum (HA, LN, PC III, and Col IV), and inhibit the expression of desmin, vimentin, and HYP content in the liver. Analyzing the results of network pharmacology, the oxidative stress, inflammation, and the related pathways (primarily the TNF signaling pathway) were identified as the potential mechanism of HJRG against liver fibrosis. Experiments confirmed that HJRG can significantly increase the content of superoxide dismutase and glutathione and reduce the levels of malondialdehyde and myeloperoxidase in the rat liver; in addition, HJRG significantly inhibited the content of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) and reduced the expression of inflammatory regulators (Cox2 and iNOS). Meanwhile, treatment with HJRG inhibited the phosphorylation of NF-κB P65, IκBα, ERK, JNK, and MAPK P38. Moreover, HJRG treatment reversed the increased expression of TNFR1. The Huangjia Ruangan granule can effectively inhibit liver fibrosis through antioxidation, suppressing liver inflammation by regulating the TNF/MAPK and NF-κB signaling pathways, thereby preventing the effect of liver fibrosis.

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Hepatoprotective, antioxidant and, anti-inflammatory potentials of gallic acid in carbon tetrachloride-induced hepatic damage in Wistar rats

Cited by 58 publications

References 42 publications

Polyphenols from Green tea revert CCl4-Induced liver oxidative stress and inflammation associated with high fat diet by activation of NRF-2 and TIMP-1 pathways to neutralize ROS

Polyphenols from Green tea revert CCl4-Induced liver oxidative stress and inflammation associated with high fat diet by activation of NRF-2 and TIMP-1 pathways to neutralize ROS

Effect of tannic acid-templated mesoporous silica nanoparticles on iron-induced oxidative stress and liver toxicity in rats

Huangjia Ruangan Granule Inhibits Inflammation in a Rat Model with Liver Fibrosis by Regulating TNF/MAPK and NF-κB Signaling Pathways

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