Hepatoprotective effect of methanolic Tanacetum parthenium extract on CCl4-induced liver damage in rats

Mahmoodzadeh, Yavar; Mazani, Mohammad; Rezagholizadeh, Lotfollah

doi:10.1016/j.toxrep.2017.08.003

Cited by 76 publications

(66 citation statements)

References 36 publications

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“…The etahnolic extract of C. oliviforme (Oe) could thus be considered as the most effective in reversing the harmful effect of CCl 4 -liver injury on ALT and AST raised levels when compared to the standard hepatoprotective drug, Silymarin with relative potencies 1.51 and 2.22, respectively ( Table 2). The raised activity of serum transaminases in CCl 4 intoxicated rats, as observed in the present study, can be attributed to the damaged structural integrity of liver cells and leakage of AST and ALT enzymes into circulation [35,36]. The tendency of these marker enzymes to return to near normalcy indicates hepatocyte regeneration [37].…”

Section: Antioxidant Activities and Liver Function Parameterssupporting

confidence: 72%

Phenolic Constituents of Chrysophyllum oliviforme L. Leaf Down-Regulate TGF-β Expression and Ameliorate CCl4-Induced Liver Fibrosis: Evidence from In Vivo and In Silico Studies

et al. 2019

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The prevalence of hepatic diseases globally and in Egypt particularly necessitates an intensive search for natural hepatoprotective candidates. Despite the traditional use of Chrysophyllum oliviforme L. and C. cainito L. leaves in the treatment of certain ailments, evidence-based reports on their bioactivities are limited. In this work, in vivo and in silico studies were conducted to evaluate their methanol extracts potential to alleviate liver damage in CCl4-intoxicated rats, in addition to their antioxidant activity and identifying the molecular mechanisms of their phenolic constituents. The extracts restored the altered total cholesterol (TC), triglycerides (TG), high-density lipoproteins (HDL), alanine aminotransferase ALT, aspartate aminotransferase AST, total protein, and albumin. Histopathological architecture, DNA fragmentation, and mRNA expression level of TGF-β1 also confirmed the anti-fibrotic activity of the two extracts. The total phenolic content (TPC) in C. oliviforme ethanol extract exceeded that in C. caimito. Additionally, the malondialdehyde (MDA), reduced glutathione (GSH), and total antioxidant capacity (TAC) levels assured the antioxidant potential. Seven phenolics; quercetin, isoquercitrin, myricetin, kaempferol, and caffeic, trans-ferulic, and gallic acids were isolated from the ethanol extract of C. oliviforme. The molecular docking of isolated compounds revealed a low binding energy (kcal/mol with TGF-β1, thus confirming the hepatoprotctive activity of the extracts. In conclusion, the C. oliviforme leaves could be considered as potent safe raw material for the production of herbal formulations to alleviate hepatic toxicity after preclinical safety study.

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Section: Antioxidant Activities and Liver Function Parameterssupporting

confidence: 72%

Phenolic Constituents of Chrysophyllum oliviforme L. Leaf Down-Regulate TGF-β Expression and Ameliorate CCl4-Induced Liver Fibrosis: Evidence from In Vivo and In Silico Studies

et al. 2019

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“…Several pro-apoptotic and anti-apoptotic proteins such as Bax and Bcl2 are responsible for cellular apoptosis [61][62][63][64]. Bax is an important pro-apoptotic gene in the Bcl2 family, which may translocate to the mitochondria to induce apoptosis [65], whereas Bcl2 is an anti-apoptotic protein that suppresses apoptosis [66,67]. In our study, we found that CCl 4 administration induced apoptosis of liver cells by significant elevation of cleaved caspase-3, cleaved caspase-9 and Bax expression while Bcl2 expression was inhibited, and these conditions were reversed in DIM pretreatment condition.…”

Section: Discussionmentioning

confidence: 99%

Indole-3-Carbinol Derivative DIM Mitigates Carbon Tetrachloride-Induced Acute Liver Injury in Mice by Inhibiting Inflammatory Response, Apoptosis and Regulating Oxidative Stress

Munakarmi

Chand

Shin

et al. 2020

IJMS

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3,3′-Diindolylmethane (DIM), a metabolic product of indole-3-carbinol extracted from cruciferous vegetables exhibits anti-inflammatory and anti-cancer properties. Earlier, the product has been demonstrated to possess anti-fibrotic properties; however, its protective effects on liver injury have not been clearly elucidated. In this study, we postulated the effects and molecular mechanisms of action of DIM on carbon tetrachloride (CCl4)-induced liver injury in mice. Acute liver injury was induced by a single intraperitoneal administration of CCl4 (1 ml/kg) into mice. DIM was injected via subcutaneous route for three days at various doses (2.5, 5 and 10 mg/kg) before CCl4 injection. Mice were sacrificed and serum was collected for quantification of serum transaminases. The liver was collected and weighed. Treatment with DIM significantly reduced serum transaminases levels (AST and ALT), tumor necrosis factor-α (TNF-α) and reactive oxygen species (ROS). CCl4- induced apoptosis was inhibited by DIM treatment by the reduction in the levels of cleaved caspase-3 and Bcl2 associated X protein (Bax). DIM treated mice significantly restored Cytochrome P450 2E1, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression in CCl4 treated mice. In addition, DIM downregulated overexpression of hepatic nuclear factor kappa B (NF-κB) and inhibited CCl4 mediated apoptosis. Our results suggest that the protective effects of DIM against CCl4- induced liver injury are due to the inhibition of ROS, reduction of pro-inflammatory mediators and apoptosis.

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“…Bax is a key master apoptotic protein, while Bcl-2 is enemy of apoptosis. [61][62][63] Our realities demonstrated that CCl 4 persuaded observable apoptosis of liver cells, checked by the significant height of caspase-3 action. In concurrence with prior research, CCl 4 intensified Bax expression while diminished Bcl-2 expression.…”

Section: Discussionmentioning

confidence: 61%

“…The family incorporates proapoptotic and against apoptotic individuals. Bax is a key master apoptotic protein, while Bcl‐2 is enemy of apoptosis . Our realities demonstrated that CCl 4 persuaded observable apoptosis of liver cells, checked by the significant height of caspase‐3 action.…”

Section: Discussionmentioning

confidence: 67%

Combination of metformin and luteolin synergistically protects carbon tetrachloride‐induced hepatotoxicity: Mechanism involves antioxidant, anti‐inflammatory, antiapoptotic, and Nrf2/HO‐1 signaling pathway

Yang¹,

Yang²,

Jiangmei³

2019

BioFactors

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Liver diseases are one of the fatal disorders due to the vital role of the liver. Carbon tetrachloride (CCl4) is the most perceived chemical substance utilized in developing models of hepatic damage. Metformin (Met) is a potent antidiabetic and redox modulatory agent that has shown anticancer and protective effects on various organs. Therefore, addition of therapy with natural antioxidative agents or herbal extracts shows defensive impacts against different injuries inside the body. Luteolin (Lut) can be found in several customary Chinese remedies. It has been reported for various pharmacological actions such as antitumor, antioxidative, and anti‐inflammatory impacts. Here, the liver injury rat model was established using CCl4 (1.00 mL/kg body weight) in vivo. The protective roles of Met and Lut separately or in combination were observed in hepatotoxicity induced by CCl4. The result was shown that both Met and Lut, while individually used, were normally active in diminishing CCl4‐caused hepatotoxicity. The combination of two drugs performed synergistically to improve liver damage caused by CCl4, as shown by the considerably improved liver dysfunction. Met and Lut showed highly antioxidative effects on CCl4‐treated rats moderately by increasing the activities and expression of the antioxidant enzymes. Along with this, a combination of Met and Lut significantly suppressed inflammatory responses, which is evidenced by the reduced level of inflammatory cytokines together with interleukin 1 beta (IL‐1β), tumor necrosis factor alpha (TNF‐α), and interleukin 6 (IL‐6). Additionally, CCl4‐agitated apoptosis was intensely reduced by Met and Lut through reducing cleaved caspase‐3 and Bax (pro‐apoptotic factor) while increasing Bcl‐2 (antiapoptotic factor) signaling pathways. Cotreatments of Met and Lut upregulated nuclear factor erythroid 2‐related factor 2 (NRF2) and heme oxygenase‐1 (HO‐1) expression in the CCl4‐intoxicated rat's liver. The above result recommended that combination of Met and Lut may have a substantial potential and synergizing impact against CCl4‐induced hepatotoxicity.

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Hepatoprotective effect of methanolic Tanacetum parthenium extract on CCl4-induced liver damage in rats

Abstract: Graphical abstract

Cited by 76 publications

References 36 publications

Phenolic Constituents of Chrysophyllum oliviforme L. Leaf Down-Regulate TGF-β Expression and Ameliorate CCl4-Induced Liver Fibrosis: Evidence from In Vivo and In Silico Studies

Phenolic Constituents of Chrysophyllum oliviforme L. Leaf Down-Regulate TGF-β Expression and Ameliorate CCl4-Induced Liver Fibrosis: Evidence from In Vivo and In Silico Studies

Indole-3-Carbinol Derivative DIM Mitigates Carbon Tetrachloride-Induced Acute Liver Injury in Mice by Inhibiting Inflammatory Response, Apoptosis and Regulating Oxidative Stress

Combination of metformin and luteolin synergistically protects carbon tetrachloride‐induced hepatotoxicity: Mechanism involves antioxidant, anti‐inflammatory, antiapoptotic, and Nrf2/HO‐1 signaling pathway

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