Dicranostiga leptopodu (Maxim.) Fedde extracts attenuated CCl4-induced acute liver damage in mice through increasing anti-oxidative enzyme activity to improve mitochondrial function

Tang, Deping; Fang, Wang; Tang, Jinzhou; Mao, Aihong; Liao, Shiqi; Wang, Qin

doi:10.1016/j.biopha.2016.11.097

Cited by 11 publications

(6 citation statements)

References 23 publications

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“…CCl 4 is a hepatotoxic agent widely used in preclinical animal studies [27]. Since administration of CCl 4 can induce acute or chronic liver injury in rodents, it is extensively used as an experimental model [28]. When CCl 4 enters into the animal body, it produces trichloromethyl free radicals and reactive oxygen species (ROS) after being metabolized by cytochrome P450 [29,30].…”

Section: Discussionmentioning

confidence: 99%

Oral Delivery of Curcumin Polymeric Nanoparticles Ameliorates CCl4-Induced Subacute Hepatotoxicity in Wistar Rats

Marslin

Prakash

et al. 2018

Polymers

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Curcumin is the major bioactive compound of Curcuma longa, an important medicinal plant used in traditional herbal formulations since ancient times. In the present study, we report that curcumin nanoparticles (ηCur) protects Wistar rats against carbon tetrachloride (CCl4)-induced subacute hepatotoxicity. Nanoparticles of sizes less than 220 nm with spherical shape were prepared using PLGA and PVA respectively as polymer and stabilizer. Test animals were injected via intraperitoneal route with 1 mL/kg CCl4 (8% in olive oil) twice a week over a period of 8 weeks to induce hepatotoxicity. On the days following the CCl4 injection, test animals were orally administered with either curcumin or its equivalent dose of ηCur. Behavioural observation, biochemical analysis of serum and histopathological examination of liver of the experimental animals indicated that ηCur offer significantly higher hepatoprotection compared to curcumin.

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Section: Discussionmentioning

confidence: 99%

Oral Delivery of Curcumin Polymeric Nanoparticles Ameliorates CCl4-Induced Subacute Hepatotoxicity in Wistar Rats

Marslin

Prakash

et al. 2018

Polymers

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“…diseases, including chronic liver disease, via increased production of reactive oxygen species (ROS) that damage various organs, including the liver, has been reported (9). The mitochondrion is a vital organelle in eukaryotic cells, supplying the energy for numerous biological functions via oxidative phosphorylation.…”

Section: Riboflavin Ameliorates Mitochondrial Dysfunction Via the Amp...mentioning

confidence: 99%

Riboflavin ameliorates mitochondrial dysfunction via the AMPK/PGC1α/HO‑1 signaling pathway and attenuates carbon tetrachloride‑induced liver fibrosis in rats

et al. 2022

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Hepatic fibrosis is a global health problem, with increasing evidence demonstrating that oxidative stress serves a pivotal role in fibrogenesis. Riboflavin is a vital nutrient in the human and animal diet, which enhances the activity of antioxidant enzymes and ameliorates oxidative stress. The present study evaluated the effect of riboflavin on liver fibrosis and the mechanisms underlying this process. Rats were subcutaneously injected with carbon tetrachloride (CCl 4 ) dissolved in sterile olive oil twice per week to induce hepatic fibrosis. The effect of riboflavin on CCl 4 -induced liver fibrosis was then assessed. Blood samples and liver tissues were collected and analyzed. The liver tissue morphological changes, immunohistochemical analysis, levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in the mitochondria, and the protein expression levels of α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1), extracellular signal-regulated kinase (ERK), p38, c-Jun N-terminal kinase (JNK), AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and heme oxygenase 1 (HO-1) in the liver were also analyzed. The results demonstrated that riboflavin treatment significantly decreased the levels of alanine transaminase and aspartate transaminase in the serum, increased SOD activity and modulated the MDA level in the mitochondria. Furthermore, riboflavin significantly inhibited the CCl 4 -induced, upregulated protein expression levels of phosphorylated (p)-ERK, p-p38, p-JNK, TGF-β1 and α-SMA. Moreover, riboflavin significantly increased the expression of p-AMPK, PGC-1α and HO-1 in the liver tissue. These results suggested that riboflavin delays CCl 4 -induced hepatic fibrosis by enhancing the mitochondrial function via the AMPK/PGC-1α/HO-1 and mitogen-activated protein kinase signaling pathways.

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“…The carbon tetrachloride (CCl 4 )—induced hepatotoxicity model is one of the most extensively used in vivo models. It is now recognized that CCl 4 is a chemical hepatotoxin that can cause oxygen free radical-induced liver damage [ 4 , 5 ]. Oxidative damage and an inflammatory response are caused by CCl 4 metabolism, which in turn causes severe liver damage and hepatocyte damage associated with necrosis and apoptosis [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

The Liver Protection Effects of Maltol, a Flavoring Agent, on Carbon Tetrachloride-Induced Acute Liver Injury in Mice via Inhibiting Apoptosis and Inflammatory Response

et al. 2018

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The purpose of this research was to evaluate whether maltol could protect from hepatic injury induced by carbon tetrachloride (CCl4) in vivo by inhibition of apoptosis and inflammatory responses. In this work, maltol was administered at a level of 100 mg/kg for 15 days prior to exposure to a single injection of CCl4 (0.25%, i.p.). The results clearly indicated that the intrapulmonary injection of CCl4 resulted in a sharp increase in serum aspartate transaminase (AST) and alanine transaminase (ALT) activities, tumor necrosis factor-α (TNF-α), irreducible nitric oxide synthase (iNOS), nuclear factor-kappa B (NF-κB) and interleukin-1β (IL-1β) levels. Histopathological examination demonstrated severe hepatocyte necrosis and the destruction of architecture in liver lesions. Immunohistochemical staining and western blot analysis suggested an accumulation of iNOS, NF-κB, IL-1β and TNF-α expression. Maltol, when administered to mice for 15 days, can significantly improve these deleterious changes. In addition, TUNEL and Hoechst 33258 staining showed that a liver cell nucleus of a model group diffused uniform fluorescence following CCl4 injection. Maltol pretreatment groups did not show significant cell nuclear condensation and fragmentation, indicating that maltol inhibited CCl4-induced cell apoptosis. By evaluating the liver catalase (CAT), glutathione (GSH), superoxide dismutase (SOD) activity, and further using a single agent to evaluate the oxidative stress in CCl4-induced hepatotoxicity by immunofluorescence staining, maltol dramatically attenuated the reduction levels of hepatic CAT, GSH and SOD, and the over-expression levels of CYP2E1 and HO-1. In the mouse model of CCl4-induced liver injury, we have demonstrated that the inflammatory responses were inhibited, the serum levels of ALT and AST were reduced, cell apoptosis was suppressed, and liver injury caused by CCl4 was alleviated by maltol, demonstrating that maltol may be an efficient hepatoprotective agent.

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Dicranostiga leptopodu (Maxim.) Fedde extracts attenuated CCl4-induced acute liver damage in mice through increasing anti-oxidative enzyme activity to improve mitochondrial function

Cited by 11 publications

References 23 publications

Oral Delivery of Curcumin Polymeric Nanoparticles Ameliorates CCl4-Induced Subacute Hepatotoxicity in Wistar Rats

Oral Delivery of Curcumin Polymeric Nanoparticles Ameliorates CCl4-Induced Subacute Hepatotoxicity in Wistar Rats

Riboflavin ameliorates mitochondrial dysfunction via the AMPK/PGC1α/HO‑1 signaling pathway and attenuates carbon tetrachloride‑induced liver fibrosis in rats

The Liver Protection Effects of Maltol, a Flavoring Agent, on Carbon Tetrachloride-Induced Acute Liver Injury in Mice via Inhibiting Apoptosis and Inflammatory Response

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