Therapeutic potential of Vanillylacetone against CCl4 induced hepatotoxicity by suppressing the serum marker, oxidative stress, inflammatory cytokines and apoptosis in Swiss albino mice

Alam, Mohammad Firoz; Safhi, Mohammed M.; Anwer, Tarique; Siddiqui, Rahimullah; Khan, Gyas; Moni, Sivakumar Sivagurunathan

doi:10.1016/j.yexmp.2018.06.001

Cited by 27 publications

(18 citation statements)

References 35 publications

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“…IL-2 utilizes the actions via the IL-2R α , IL-2 R β , and IL-2R γ receptor-mediated JAK/STAT pathway. An earlier report suggested that soluble IL-2R was involved in activating immune cells in various inflammatory disease conditions [18]; elevated soluble IL-2R has been described for diverse hepatic disorders [19]. The present study suggests that the IL-2 level increased in the group of animals that received STZ, confirming the induction of hepatic injury which was also reflected in the various enzyme parameter studies.…”

Section: Discussionsupporting

confidence: 83%

Hepatoprotective Potential ofSargassum muticumagainst STZ-Induced Diabetic Liver Damage in Wistar Rats by Inhibiting Cytokines and the Apoptosis Pathway

Safhi

Alam

Moni

et al. 2019

Analytical Cellular Pathology

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Liver inflammation and necrosis are the foremost problems interlinked with diabetes mellitus (DM). The methanolic extract of Sargassum muticum (MESM) plays a hepatoprotective role in streptozotocin- (STZ-) induced hepatic injury. In this study, STZ exposure induced diabetes that augmented hepatic damage, which was reflected in serum enzyme markers, the cytokine network, and caspase-3 and caspase-9 levels in Group 2. Exposure to the MESM tremendously modulated the levels of hepatic enzyme markers ALP, ACP, ALT, and AST in Groups 3 and 4. The cytokine network was well regulated by suppressing the release of cytokines, and the levels of caspase-3 and caspase-9 were also reduced in Groups 3 and 4. The present study suggests that MESM treatment at 200 and 500 mg protected the liver and also minimizes the glucose level. Thus, the MESM plays a key role in rejuvenating the liver and can modulate diabetes’s pathogenic effect by reducing the glucose level.

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Section: Discussionsupporting

confidence: 83%

Hepatoprotective Potential ofSargassum muticumagainst STZ-Induced Diabetic Liver Damage in Wistar Rats by Inhibiting Cytokines and the Apoptosis Pathway

Safhi

Alam

Moni

et al. 2019

Analytical Cellular Pathology

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“…As the first cellular response to liver toxic damage, hepatocyte apoptosis is one of the key contributing factors for the development of acute liver injury and is also a significant feature in CCl 4 -induced liver injury [ 17 , 22 , 23 ]. The results from terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) assay confirmed that CCl 4 challenge induced massive hepatocyte apoptosis; importantly, pre-treatment with low-, high-dose eckol, or bifendate greatly reduced the number of TUNEL-positive apoptotic hepatocytes ( Figure 3 A).…”

Section: Resultsmentioning

confidence: 99%

“…Here, we also found the protective effect of eckol on hepatocyte apoptosis induced by CCl 4 . Considering the important role of hepatocyte apoptosis in CCl 4 -induced liver injury [ 17 , 22 , 23 ], it is reasonable to assume that eckol could function as an anti-apoptotic agent with a subsequent hepato-protective effect.…”

Section: Resultsmentioning

confidence: 99%

“…In addition, CCl 4 exposure could trigger the production of inflammatory cytokines and chemokines, stimulating the recruitment of inflammatory cells [ 16 ]. Moreover, as another crucial event involved in the acute liver injury induced by CCl 4 , apoptosis is a programmed cell death leading to morphological changes and death in the hepatocytes [ 17 ]. Accordingly, antioxidant, anti-inflammatory and anti-apoptosis therapies have been shown to have desirable effects for prevention or treatment of liver diseases in animal models, and to be clinically effective in preventing the disease progress or improving the outcome of patients [ 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

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Protective Effect of Eckol against Acute Hepatic Injury Induced by Carbon Tetrachloride in Mice

Liu

Zhang

et al. 2018

Marine Drugs

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Several in vitro studies have shown the potential hepatoprotective properties of eckol, a natural phlorotannin derived from the brown alga. However, the in vivo hepatoprotective potential of eckol has not been determined. In this study, we performed an in vivo study to investigate the protective effect of eckol and its possible mechanisms on the carbon tetrachloride (CCl4)-induced acute liver injury model in mice. Results revealed that eckol pre-treatment at the dose of 0.5 and 1.0 mg/kg/day for 7 days significantly suppressed the CCl4-induced increases of alanine transaminase (ALT) and aspartate aminotransferase (AST) levels in serum and meliorated morphological liver injury. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) analysis showed that the number of positive apoptotic hepatocytes in the eckol-treated group was lower than that in the CCl4 model group. Western blotting analysis also demonstrated the enhanced expression of bcl-2 and suppressed expression of cleaved caspase-3 by eckol. The CCl4-induced oxidative stress in liver was significantly ameliorated by eckol, which was characterized by reduced malondialdehyde (MDA) formations, and enhanced superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities and glutathione (GSH) content. Moreover, the CCl4-induced elevations of pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were markedly suppressed in the eckol-treated group. However, eckol enhanced the level of IL-10, a potent anti-inflammatory cytokine, and recruited CD11c+ dendritic cells into the liver tissues of CCl4-treated mice. These results indicated that eckol has the protective effect on CCl4-induced acute liver injury via multiple mechanisms including anti-apoptosis, anti-oxidation, anti-inflammation and immune regulation.

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“…Apoptosis, similarly is the programmed cell death that could be attributed to oxidative stress and accumulation of free radicals. Apoptosis is the main cell death mechanism recognized following the induction of CCl 4 liver injury [13,14]. Consequently, anti-oxidant and anti-apoptosis therapies exhibited desirable effects for prevention or treatment of liver diseases in animal models [15,16].…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Flavone from Tamarix aphylla against CCl4-Induced Liver Injury in Mice Mediated by Suppression of Oxidative Stress, Apoptosis and Angiogenesis

El‐Aarag

Khairy

Khalifa

et al. 2019

IJMS

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The current study aimed to investigate, for the first time, the beneficial effects of 3,5-dihydroxy-4′,7-dimethoxyflavone isolated from Tamarix aphylla L. against liver injury in mice. Liver injury was induced by intraperitoneal (i.p.) injection of carbon tetrachloride (CCl4) at a dose of 0.4 mL/kg mixed in olive oil at ratio (1:4) twice a week for 6 consecutive weeks. The administration of CCl4 caused significant histopathological changes in liver tissues while the pre-treatment with the flavone at dose of 10 and 25 mg/kg ameliorated the observed liver damages. Also, it markedly reduced hepatic malondialdehyde (MDA) level as well as increased the activities of liver superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (Gpx) compared with their recorded levels in CCl4 model group. Moreover, the immunohistochemical analysis demonstrated the enhancement in the protein level of B-cell lymphoma-2 (Bcl-2) while the protein levels of cysteine-aspartic acid protease-3 (caspase-3), Bcl-2-associated x protein (Bax), transforming growth factor-β1 (TGF-β1) and CD31 were suppressed following the flavone treatement. These results suggest that the flavone can inhibit liver injury induced in mice owning to its impact on the oxidation, apoptotic and angiogenesis mechanisms. Further pharmacological investigations are essential to determine the effectiveness of the flavone in human.

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Therapeutic potential of Vanillylacetone against CCl4 induced hepatotoxicity by suppressing the serum marker, oxidative stress, inflammatory cytokines and apoptosis in Swiss albino mice

Cited by 27 publications

References 35 publications

Hepatoprotective Potential ofSargassum muticumagainst STZ-Induced Diabetic Liver Damage in Wistar Rats by Inhibiting Cytokines and the Apoptosis Pathway

Hepatoprotective Potential ofSargassum muticumagainst STZ-Induced Diabetic Liver Damage in Wistar Rats by Inhibiting Cytokines and the Apoptosis Pathway

Protective Effect of Eckol against Acute Hepatic Injury Induced by Carbon Tetrachloride in Mice

Protective Effects of Flavone from Tamarix aphylla against CCl4-Induced Liver Injury in Mice Mediated by Suppression of Oxidative Stress, Apoptosis and Angiogenesis

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