The Protective Effect of Garden Cress Lepidium sativum against Lipopolysaccharide (LPS) Induced Hepatotoxicity in Mice Model

2021 ◽  
Author(s):  
Abdalla A. Sayed ◽  
Ali M. Ali ◽  
Gamal M. Bekhet
Keyword(s):  
Liver Injury ◽  
Biochemical Analysis ◽  
White Male ◽  
Protective Role ◽  
Oxidative Enzymes ◽  
Lepidium Sativum ◽  
Experimental Investigations ◽  
Control Group ◽  
Mice Model ◽  
Histopathological Studies

Background: Lepidium sativum (LS) is a very potent and often used as anti-cancer is largely limited due to the dose-related toxic effects. The present study investigated the protective role of LS that can reduce the liver injury induced by LPS.Methods: Forty white male mice were randomly divided into five groups: the vehicle control group, LPS group, LPS plus LS group, LS pretreated plus LPS group and LS + LPS + LS group. Mice were sacrificed at 2, 4, 8, 16, 24 and 48h. Blood and liver samples were collected for the experimental investigations. Biochemical analysis, histopathological studies and molecular investigation carried out for different groups used. Result: Biochemical analysis for serum AST, ALT, LDL and HDL levels were determined to evaluate liver status. Oxidative stress of liver examined through determination of oxidative enzymes. Furthermore, proinflammatory (IL-6 and TNF-α) and anti-inflammatory (IL-4 and IL-10) cytokines were investigated. Histopathological liver sections were examined to show the alterations due to LPS injection. Biochemical analysis showed a significant modulatory effect of LS on the LPS challenged mice. Histopathological studies showed that LPS caused liver alterations, such as necrosis, infiltrations of neutrophils, sinusoid congestion and hepatocellular degeneration in the liver. These histopathological modulations were significant by LS pretreatment. These findings indicate that LS has a significant hepatoprotective effect on LPS-induced liver injury in mice model.

scholarly journals Protective Role of Coenzyme Q10 in Acute Sepsis-Induced Liver Injury in BALB/c Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Qian-wei Li ◽  
Qin Yang ◽  
Hong-Yang Liu ◽  
Yu-ling Wu ◽  
Yu-Hua Hao ◽  
...  
Keyword(s):  
Liver Injury ◽  
Coenzyme Q10 ◽  
Cecal Ligation ◽  
Protective Role ◽  
Hepatic Tissue ◽  
Control Group ◽  
Cecal Ligation And Puncture ◽  
Sequestosome 1

Sepsis increases the risk of the liver injury development. According to the research works, coenzyme Q10 exhibits hepatoprotective properties in vivo as well as in vitro. Current work aimed at investigating the protective impacts of coenzyme Q10 against liver injury in septic BALB/c mice. The male BALB/c mice were randomly segregated into 4 groups: the control group, the coenzyme Q10 treatment group, the puncture and cecal ligation group, and the coenzyme Q10+cecal ligation and puncture group. Cecal ligation and puncture was conducted after gavagaging the mice with coenzyme Q10 during two weeks. Following 48 h postcecal ligation and puncture, we estimated hepatic biochemical parameters and histopathological changes in hepatic tissue. We evaluated the expression of factors associated with autophagy, pyroptosis, and inflammation. Findings indicated that coenzyme Q10 decreased the plasma levels in alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase in the cecal ligation and puncture group. Coenzyme Q10 significantly inhibited the elevation of sequestosome-1, interleukin-1β, oligomerization domain-like receptor 3 and nucleotide-binding, interleukin-6, and tumor necrosis factor-α expression levels; coenzyme Q10 also increased beclin 1 levels. Coenzyme Q10 might be a significant agent in the treatment of liver injury induced by sepsis.

scholarly journals Effects of Exposure to Aflatoxin G1 on the Plasma Biochemical Factors and Histopathological Properties of Renal Tissue in Mice

2021 ◽  
Vol 15 (2) ◽  
pp. 127-134
Author(s):  
Touraj Zamir-Nasta ◽  
◽  
Arash Ahmadi ◽  
Moein Yazdkhasti ◽  
Mona Pazhouhi ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Biochemical Analysis ◽  
Plasma Concentrations ◽  
Renal Tissue ◽  
Control Group ◽  
Male Mice ◽  
Blood Samples ◽  
Aquaporin 1 ◽  
Histopathological Studies ◽  
Sodium And Potassium

Background: Among aflatoxins, the subtype aflatoxin G1 is one of the most toxic, commonly found in cereals, legumes, dairy and non-alcoholic beers. Aflatoxins have been known as nephrotoxic compounds. In this study, changes in the expression of aquaporin-1, the histopathology of renal tissue and plasma biochemical factors after exposure to aflatoxin G1 were investigated in mice. Methods: Twenty-four adult male mice (weighing 20±2 g) were divided into four groups of six. The control group received the vehicle (0.2 ml) and the three experimental groups were injected intraperitoneally with aflatoxin G1 at 20 μg/kg for 7, 15 or 35 days, respectively. On days 7, 15 and 35, blood samples were drawn from the mice for biochemical analysis of plasma and the kidney tissues were sampled for real-time PCR and histopathological studies. Results: The real PCR results showed a reduction in aquaporin-1 expression in the experimental groups compared to those in the controls (P<0.05). Also, the plasma concentrations of urea and creatinine were significantly increased in the experimental groups compared to those in the controls (P<0.05). Also, the serum sodium and potassium levels had decreased significantly compared to the controls (P<0.05). Various damages were observed in the ureters and glomeruli among the experimental groups compared to those in the controls. Conclusion: Aflatoxin G1 had adverse effects on the renal tissue by reducing the expression of aquaporin-1. Subsequently, there were biochemical manifestations in the serum, consisting of changes in the concentrations of urea, creatinine, sodium and potassium, confirming the histopathological toxicity of aflatoxin G1.

scholarly journals Hepatic progenitor cells promote the repair of schistosomiasis liver injury by inhibiting IL-33 secretion in mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Beibei Zhang ◽  
Xiaoying Wu ◽  
Jing Li ◽  
An Ning ◽  
Bo Zhang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Progenitor Cells ◽  
Normal Liver ◽  
Protective Role ◽  
Dependent Manner ◽  
Hepatic Progenitor Cells ◽  
Wild Type ◽  
Mice Model

Abstract Background Hepatic schistosomiasis, a chronic liver injury induced by long-term Schistosoma japonicum (S. japonicum) infection, is characterized by egg granulomas and fibrotic pathology. Hepatic progenitor cells (HPCs), which are nearly absent or quiescent in normal liver, play vital roles in chronic and severe liver injury. But their role in the progression of liver injury during infection remains unknown. Methods In this study, the hepatic egg granulomas, fibrosis and proliferation of HPCs were analyzed in the mice model of S. japonicum infection at different infectious stages. For validating the role of HPCs in hepatic injury, tumor necrosis factor-like-weak inducer of apoptosis (TWEAK) and TWEAK blocking antibody were used to manipulate the proliferation of HPCs in wild-type and IL-33−/− mice infected with S. japonicum. Results We found that the proliferation of HPCs was accompanied by inflammatory granulomas and fibrosis formation. HPCs expansion promoted liver regeneration and inhibited inflammatory egg granulomas, as well as the deposition of fibrotic collagen. Interestingly, the expression of IL-33 was negatively associated with HPCs’ expansion. There were no obvious differences of liver injury caused by infection between wild-type and IL-33−/− mice with HPCs’ expansion. However, liver injury was more attenuated in IL-33−/− mice than wild-type mice when the proliferation of HPCs was inhibited by anti-TWEAK. Conclusions Our data uncovered a protective role of HPCs in hepatic schistosomiasis in an IL-33-dependent manner, which might provide a promising progenitor cell therapy for hepatic schistosomiasis.

scholarly journals Epigallocatechin-3-Gallate (EGCG), An Active Constituent of Green Tea: Implications in the Prevention of Liver Injury Induced by Diethylnitrosamine (DEN) in Rats

2019 ◽  
Vol 9 (22) ◽  
pp. 4821 ◽  
Author(s):  
Saleh A. Almatroodi ◽  
Mohammed A. Alsahli ◽  
Hanan Marzoq Alharbi ◽  
Amjad Ali Khan ◽  
Arshad Husain Rahmani
Keyword(s):  
Cell Cycle ◽  
Liver Injury ◽  
Green Tea ◽  
Liver Toxicity ◽  
Oxidative Capacity ◽  
Oxidative Enzymes ◽  
Control Group ◽  
Active Constituent ◽  
Drug Induced ◽  
Oxidative Potential

Liver diseases are one of the most detrimental conditions that may cause inflammation, leading to tissue damage and perturbations in functions. Several drugs are conventionally available for the treatment of such diseases, but the emergence of resistance and drug-induced liver injury remains pervasive. Hence, alternative therapeutic strategies have to be looked upon. Epigallocatechin-3-gallate (EGCG) is a naturally occurring polyphenol in green tea that has been known for its disease-curing properties. In this study, we aimed to evaluate its anti-oxidative potential and protective role against diethylnitrosamine (DEN)-induced liver injury. Four different groups of rats were used for this study. The first group received normal saline and served as the control group. The second group received DEN (50 mg/kg body wt) alone and third group received DEN plus EGCG (40 mg/kg body wt) only. The fourth group were treated with EGCG only. The liver protective effect of EGCG against DEN toxicity through monitoring the alterations in aspartate transaminase (AST), and alanine transaminase (ALT) and alkaline phosphatase (ALP) activities, serum level of pro-inflammatory mediators and anti-oxidant enzymes, histopathological alterations, measurement of cellular apoptosis, and cell cycle analysis was examined. The rats that were given DEN only had a highly significantly elevated levels of liver enzymes and pro-inflammatory cytokines, highly decreased anti-oxidative enzymes, and histological changes. In addition, a significant elevation in the percentage of apoptotic nuclei and cell cycle arrest in the sub- G1 phase was detected. EGCG acts as a hepatoprotectant on DENs by reducing the serum levels of liver functional enzymes, increasing total anti-oxidative capacity, reducing pathological changes and apoptosis, as well as causing the movement of cells from the sub G1 to S or G2/M phase of the cell cycle. In conclusion, EGCG displayed a powerful hepatoprotective additive as it considerably mitigates the liver toxicity and apoptosis induced by DEN.

Potential Effect of β-casomorphin-7 on Lymphocyte and TLR\NF-κB Signaling Pathway in Intestinal Mucosa of Aged Mice

2020 ◽  
Author(s):  
Hong Yin ◽  
Xiaqing Su ◽  
Jijie Liu ◽  
Lihua Li ◽  
Lihua Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Intestinal Mucosa ◽  
The Elderly ◽  
Potential Effect ◽  
Protective Role ◽  
Control Group ◽  
Relative Expression ◽  
Aged Mice ◽  
Histopathological Studies

The effect of â-Casomorphin-7 on intestinal mucosal immunity was investigated in aged mice. Mice were treated without or with different doses of â-Casomorphin-7 for 30 days. All mice were sacrificed and intestinal mucosa samples collection at the end of the experiment. Histopathological studies showed the tissue protective role of â-Casomorphin-7 in aged mice. The number of duodenal and jejunal epithelial lymphocytes decreased significantly Pandlt;0.05 The doses of duodenal and jejunal epithelial lymphocytes in mice were significantly Pandlt;0.05 increased in each dose group. The relative expression of TLR4,TRAF6 and NF-êB in the intestinal mucosa of the elderly model group was lower than that of the young control group. The low and middle dose groups significantly Pandlt;0.05 up-regulated the relative expression of TLR4, TRAF6 and NF-êB.The results suggest that â-Casomorphin-7 can improved intestinal mucosal immune decline likely through balancing TLR4\NF-êB signaling pathway.

scholarly journals Hepatic Progenitor Cells Promote the Repair of Schistosomiasis Liver Injury Through Inhibiting IL-33 Secretion 

2021 ◽  
Author(s):  
Beibei Zhang ◽  
Xiaoying Wu ◽  
Jing Li ◽  
An Ning ◽  
Bo Zhang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Progenitor Cells ◽  
Progenitor Cell ◽  
Normal Liver ◽  
Protective Role ◽  
Hepatic Progenitor Cells ◽  
Mice Model ◽  
Blocking Antibody

Abstract Background: Hepatic schistosomiasis, a chronic liver injury induced by long-term Schistosoma japonicum (S. japonicum) infection, is characterized by egg granulomas and fibrotic pathology. Hepatic progenitor cells (HPCs), which are nearly absent and quiescent in normal liver, play vital roles in chronic and severe liver injury. But their role in the progression of liver injury during infection remained unknown.Methods: In this study, the hepatic egg granulomas, fibrosis and proliferation of HPCs were analyzed in S. japonicum infection mice model at different infection stages. For validating the role of HPCs in hepatic injury, TNF­related weak inducer of apoptosis (TWEAK) and TWEAK blocking antibody were used to manipulate the proliferation of HPCs. Histologic pathology and the expression of IL-33 were examined. Results: We found that the proliferation of HPCs paralleled with inflammatory granulomas and fibrosis formation. Promoting HPCs expansion promote the liver regeneration and inhibit the hepatocytes injury, the inflammatory eggs granulomas and the deposition of fibrotic collagen. Interestingly, the expression of IL-33 decreased when HPCs were manipulated to proliferate. Thus, IL-33 might be involved in the liver repair dominated by HPCs. Conclusions: Collectively, our data uncovered a protective role of HPCs in hepatic schistosomiasis in an IL-33 related manner, which might provide a promising progenitor cell therapy for hepatic schistosomiasis.

scholarly journals Gamma (γ)-mangostin attenuated gastric ulcers induced by absolute alcohol in rats: Histological, immunohistochemical and biochemical investigation

2021 ◽  
Author(s):  
Sarwan W. Bradosty ◽  
Saber W. Hamad ◽  
Faiyaz Khudaboddin Shaikh ◽  
Nadir Mustafa Nanakali ◽  
Hero Helal Muhammed saed ◽  
...  
Keyword(s):  
Gastric Juice ◽  
Biochemical Analysis ◽  
Oral Feeding ◽  
Oxidative Enzymes ◽  
Tissue Homogenate ◽  
Tween 20 ◽  
Control Group ◽  
Absolute Alcohol ◽  
Bax Protein ◽  
Gastroprotective Effect

Abstract Garcinia mangostana L. (Clusiaceae) principally contains gamma (γ)-mangostin, a xanthone that exhibits a wide spectrum of bioactivities. The current study was aimed to establish the gastroprotective effect of this compound in ethanol-induced gastric mucosal injuries in rats. Experimental Sprague Dawley (SD) rats (n = 30) were arbitrarily alienated into 5 groups (n = 6): negative control (10% Tween 20), ulcer control (10% Tween 20 + 5ml/kg absolute alcohol), reference control (5ml/kg absolute alcohol + 20mg/kg omeprazole), and two experimental groups (5ml/kg absolute alcohol + 10mg/kg γ-mangostin and 5ml/kg absolute alcohol + 20mg/kg γ-mangostin). After successful oral feeding, all rats were anesthetized and sacrificed. Gastro-histology highlighted severe injuries to the gastric mucosa with decrease in gastric mucosal content and gastric juice pH in ulcer control group. γ-mangostin (10 mg/kg & 20 mg/kg) showed strong gastroprotective effect by enhancing gastric mucosal content and gastric juice pH compared to the ulcer group, comparable to the omeprazole. Immuno-histochemical analysis revealed that γ-mangostin found to upregulate mucosal Hsp70 protein, and down-regulate Bax proteins. The biochemical analysis of mucosal tissue homogenate showed significant antioxidant activity with increase in SOD and CAT activities, whereas MDA was significantly decreased at p < 0.001. The histological, immuno-histochemical and biochemical analysis evidenced gastroprotective effects of γ-mangostin that are attributed to its potential to inhibit alcohol induced oxidative stress. Specifically, γ-mangostin improved histology of mucosal content and enhanced anti-oxidative enzymes (SOD & CAT) with decreasing lipid peroxidation (MDA). Furthermore dose dependent administration of γ-mangostin down-regulated expression of Bax protein and up-regulated HSP70.

scholarly journals Protective role of Broccoli powder against continuous ingestion of Escitalopram antidepressant drug induced hepatotoxicity in Swiss albino male mice

2017 ◽  
Vol 9 (2) ◽  
Author(s):  
Sneha Saxena ◽  
Lata Shahani ◽  
Pradeep Bhatnagar
Keyword(s):  
Antioxidant Enzymes ◽  
Antidepressant Drug ◽  
Treated Group ◽  
Protective Role ◽  
Positive Control ◽  
Control Group ◽  
Male Mice ◽  
Drug Induced ◽  
Histopathological Studies

<p>To investigate the protective role of broccoli powder “<em>Brassica Oleracea Italica</em>” against continuous ingestion of escitalopram antidepressant drug induced hepatotoxicity in Swiss albino male mice.</p><p>Mice were divided into different groups. Group1: Normal control (0.9% NaCl), Group 2: Escitalopram drug treated only (20 mg/kg), Group 3: Broccoli powder with Escitalopram drug treated (200 mg/kg + 20 mg/kg), Group 4: Olive oil vehicle control, Group 5: Carbon tetrachloride (CCl<sub>4</sub>) referenced as positive control (33 mg/kg), Group 6: Broccoli powder with CCl<sub>4</sub> treated (200 mg/kg + 33 mg/kg). The effect of these groups on liver tissue was studied after three different time periods for 4, 8 and 12 weeks.</p>The results showed that the treatment with escitalopram drug displayed significantly increased serum SGOT, SGPT, ALP level and alter liver antioxidant enzymes level (LPO, SOD and GSH) that are comparable with CCl<sub>4</sub>intoxicated group considered as positive control. Comparing escitalopram drug treated group with group that received both broccoli powder and escitalopram drug displayed a significant decrease in serum SGOT, SGPT, ALP levels and restored the level of antioxidant enzymes. The protective effect of broccoli powder on escitalopram drug induced hepatotoxicity was also supported by histopathological studies.<p> </p>

scholarly journals UPLC-MS/MS method for simultaneously determining nucleosides and methyl-nucleosides in liver mRNA of Epimedin C-induced liver injury mouse model

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Zhizhen Song ◽  
Zeyun Li ◽  
Xueqian Wen ◽  
Ruijuan Liu ◽  
Xin Tian
Keyword(s):  
Liver Injury ◽  
Mouse Model ◽  
High Performance ◽  
Enzymatic Digestion ◽  
Control Group ◽  
Mice Model ◽  
Vacuolar Degeneration ◽  
Serum Aminotransferase ◽  
Mrna Methylation ◽  
Mice Liver

Abstract Background Epimedin C, one of the main active ingredients of Epimedium, has been reported to have potential hepatotoxicity. However, the mechanism of Epimedin C-induced liver injury has not been studied. mRNA methylation, mainly including N6-methyladenosine and N5-methylcytidine, is implicated in the regulation of many biological processes and diseases. The study of quantifying mRNA methylation alterations in Epimedin C-induced liver injury mice may contribute to clarify the mechanism of its hepatotoxicity. Therefore, an analysis method needs to be established to determine nucleoside and methyl-nucleoside levels in liver mRNA. Methods An ultra-high performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) method was developed and validated to simultaneously determine six nucleosides (adenosine, uridine, cytidine, guanosine, N6-methyladenosine and N5-methylcytidine) in liver mRNA. Besides, the Epimedin C-induced liver injury mouse model was studied by intragastrical administration Epimedin C at a daily dose of 10 or 40 mg/kg for 4 weeks. The nucleoside samples of the mice liver mRNA were prepared and separated on an UPLC column using 0.1% formic acid water and methanol after enzymatic digestion. Then the sample was detected by a Qtrap 6500 mass spectrometer. Results In this method, calibration curves of the six nucleosides showed good linearity over their concentration ranges. The linear ranges were 40–20,000 pg/mL for adenosine, cytidine, N6-methyladenosine and N5-methylcytidine, 0.2–100 ng/mL for guanosine, and 2–1000 ng/mL for uridine. Epimedin C-induced liver injury mouse model was successfully established,which could be proved by the elevation of serum aminotransferase levels, and the increased inflammatory cell infiltration as well as vacuolar degeneration in liver. The N6-methyladenosine and N5-methylcytidine levels, and the ratios of N6-methyladenosine to adenosine and N5-methylcytidine to cytidine of the mice liver mRNA were all significantly increased after Epimedin C treatment. Conclusion The established method was successfully applied to the determination of six nucleosides levels in liver mRNA of the Epimedin C-induced liver injury mice model and the control group. The results indicated that mRNA methylation might be associated with Epimedin C-induced liver injury. This study will facilitate the mechanism research on the hepatotoxicity of Epimedin C.

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