scholarly journals Protective effect of leaf extract of Ficus carica L. against carbon tetrachloride-induced hepatic toxicity in mice and HepG2 cell line

2021 ◽  
Vol 20 (1) ◽  
pp. 113-119
Author(s):  
Syeda Hira ◽  
Muhammad Gulfraz ◽  
S.M. Saqlan Naqvi ◽  
Rehmat Ullah Qureshi ◽  
Hina Gul

Purpose: To determine the in vivo and in vitro hepatoprotective effects of Ficus carica.Methods: The methanol leaf extract of Ficus carica L was further fractionated into n-hexane, ethyl acetate and aqueous fractions. For in vivo study, male albino mice were divided into twelve groups. Hepatotoxicity was induced in the mice using carbon tetrachloride (CCl4). The extract of F. carica and its fractions were administered at doses of 200 and 400 mg/kg. Silymarin was used as standardhepatoprotective drug. The protective effects of the extract and fractions were determined via assay of biochemical parameters and antioxidant enzymes in the liver. The histopathology of the liver was also studied. Moreover, the in vitro hepatoprotective effect of the extract and fractions against CCl4-induced damage was determined in HepG2 cell line.Results: There were significant increases in the serum levels of liver biomarkers in CCl4-treated group, whereas treatments with plant extract and fractions significantly reduced the levels of these parameters (p < 0.05). In addition, results from histopathology revealed evidence of protective effect of Ficus carica through reversal of CCl4-induced decreases in the activities of liver antioxidant enzymes.Conclusion: These results indicate that methanol leaf extract of Ficus carica L. and its fractions exert significant and dose-dependent hepatoprotective effects in vivo and in vitro. Keywords: Ficus carica, Hepatoprotection, Carbon tetrachloride, Liver biomarkers

Marine Drugs ◽  
2018 ◽  
Vol 16 (9) ◽  
pp. 300 ◽  
Author(s):  
Shulan Li ◽  
Juan Liu ◽  
Mengya Zhang ◽  
Yuan Chen ◽  
Tianxing Zhu ◽  
...  

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.


2018 ◽  
Vol 74 (2) ◽  
pp. 301-312 ◽  
Author(s):  
Wei Zhang ◽  
Zheng Dong ◽  
Xiujuan Chang ◽  
Cuihong Zhang ◽  
Guanghua Rong ◽  
...  

2014 ◽  
Vol 213 ◽  
pp. 51-59 ◽  
Author(s):  
Lihua Hu ◽  
Lingrui Li ◽  
Demei Xu ◽  
Xiaomin Xia ◽  
Ruxian Pi ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Heng-feng Yuan ◽  
Jian-feng Pan ◽  
Shuo Li ◽  
Chang-an Guo ◽  
Shu-hao Liu ◽  
...  

This research was designed to investigate the protective effects of TSPN on steroid-induced avascular necrosis of the femoral head (ANFH) and the likely mechanisms of those effects. As an in vivo study, TSPN was shown to be protective against steroid-induced ANFH due to the upregulation of VEGF-A. Furthermore, TSPN attenuated the apoptosis of osteocytes and reduced the expression of Caspase-3 relative to the model group. As an in vitro study, TSPN exerted a concentration-dependent protective effect against apoptosis in MC3T3-E1 cells. Moreover, TSPN (at a dose of 100 μg/mL) significantly reversed the dexamethasone-induced augmentation of Caspase-3 expression and activity. Therefore, our study demonstrated that TSPN had a protective effect against steroid-induced ANFH that was related to the upregulation of VEGF-A and the inhibition of apoptosis and Caspase-3 activation.


2020 ◽  
Vol 13 (7) ◽  
pp. 1327-1333
Author(s):  
Soukaina El-Guendouz ◽  
Soumia Zizi ◽  
Youssef Elamine ◽  
Badiaa Lyoussi

Background and Aim: Hexavalent chromium (Cr (VI)) compounds have been shown to induce nephrotoxicity associated with oxidative stress in humans and animals. The aim of the present study was to investigate the nephroprotective effect of bee propolis, as highly antioxidant natural product, in vivo using an animal model. Materials and Methods: First of all, total phenol and flavonoid contents of propolis sample were estimated in vitro. Afterward, to study the protective effect of propolis on renal damages caused by an injection of a single dose of potassium dichromate (15 mg/kg b.wt), 24 male Wister rats were divided into test and control groups. Propolis treatment was performed by oral gavage of 100 mg/kg b.wt/day, while the control groups received water instead. The 24 h urine was collected and blood samples were withdrawn before and after each treatment for further analysis. Results: Propolis revealed to be rich in polyphenols and flavonoids. Chromate provoked a nephrotoxic effect expressed by a drastic decrease in glomerular filtration assessed by creatinine clearance. However, the administration of propolis attenuated the renal damages induced by the chromate. This attenuation can be seen by the increase of creatinine clearance when comparing propolis treated group to the non-treated group. Conclusion: Propolis showed a protective potential against chromate-induced nephrotoxicity through the amelioration of chromate's toxic effects. It might be concluded that propolis could be effective as chemoprotectant in the management of potassium dichromate-induced nephrotoxicity.


Author(s):  
Zheming Shao ◽  
Qihong Shen ◽  
Min Kong ◽  
Huadong Ni ◽  
Xiaomin Hou

Acute myocardial infarction (AMI) is a heart disease that seriously threatens human health. Dexmedetomidine (DEX) has a certain protective effect on cardiac injury. This study investigated the cardioprotective effect of DEX and its potential molecular mechanism in vivo and in vitro. The results showed that DEX could significantly increase the viability of hypoxia/reoxygenation (H/R) treated cardiomyocytes and reduce oxidative damage and apoptosis. Further molecular mechanism analysis showed that the above cardiac protective effects may be related to Akt signaling pathway. In addition, the expression of G-Protein Receptor 30 (GPR30) was promoted after H/R treatment. However, knockdown of GPR30 by shRNA significantly counteracted the cardioprotective effect of DEX. Meanwhile, we constructed a rat model of AMI to investigate the role of GPR30 in vivo. The results showed that DEX significantly reduced the infarct size, and GPR30 agonist G1 enhanced the protective effect of DEX on heart. On the contrary, protein kinase B (AKT) inhibitor LY294002 counteracted the protective effect of DEX on heart, suggesting that GPR30 enhanced the protective effect of DEX on ischemia-reperfusion induced heart injury by regulating AKT related pathways. In conclusion, our study provides a potential target for the clinical treatment of AMI.


2021 ◽  
Vol 11 (18) ◽  
pp. 8758
Author(s):  
Dac Thang Hoang ◽  
Thi Thu Hien Truong ◽  
Ngo Viet Duc ◽  
Le Tuan Anh Hoang ◽  
Thi Thao Do ◽  
...  

Helicteres hirsuta Lour. is a traditional Vietnamese medicine for treating chronic liver diseases such as cirrhosis and liver cancer. Many in vitro and in vivo experiments have demonstrated that the extracts and isolated compounds from H. hirsuta have diverse pharmacological activities, including antioxidant, anti-inflammatory, and anti-cancer effects. However, the hepatoprotective effects have not been reported until now. Therefore, the methanolic and ethanolic extracts of the aerial part of the H. hirsuta L. (HHM and HHE-1/1) were examined on liver fibrosis induced by carbon tetrachloride (CCl4) in rats for the first time. The results revealed that all the livers of the model group had stage F4 cirrhosis; the group that received silymarin, and HHM and HHE-1/1 had milder liver damage cirrhosis stage F1-F2 which implies that the methanolic and ethanolic extracts of H. hirsute have a definite advantage in the development of food or oral medications for hepatoprotective activity.


1985 ◽  
Vol 230 (2) ◽  
pp. 395-402 ◽  
Author(s):  
W S Din ◽  
J M Frazier

An isolated rat hepatocyte preparation was used to study the cellular toxicity of cadmium and the protective effects of metallothionein on cadmium-induced toxicity. Exposure of primary suspension cultures of isolated rat hepatocytes to Cd2+ (0-35.7 microM) for 15 min resulted in a dose-dependent reduction in the synthesis of cellular proteins during a subsequent 6 h incubation. Such inhibition could not be correlated with cellular lethality or gross membrane damage. Pre-induction of metallothionein in hepatocytes by zinc treatment in vivo of donor rats protected hepatocytes in vitro from cadmium-induced inhibition of protein synthesis. The protective effects in zinc-pre-induced hepatocytes are not due to alterations in the level of total cellular cadmium, but could be accounted for by the redistribution of intracellular cadmium in the presence of high levels of zinc-metallothionein. The data suggest that metallothionein exerts its protective effect by a kinetic detoxification mechanism, i.e. a decrease in reactive intracellular cadmium.


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