Identification and differential expression of microRNAs associated with fat deposition in the liver of Wistar rats with nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) has become notorious globally. Increasingly emerging evidence shows that NAFLD is strongly associated with inflammation, with proinflammatory cytokines such as interleukin-2 (IL-2), interleukin-6 (IL-6), and tumour necrosis factor-α (TNF-α) playing a vital role in its progression. In this work, an attempt was made to verify the anti-inflammatory activity of Ruzu herbal bitters (RHB), an antiobesity medicinal concoction, on NAFLD induced by a high-fat diet (HFD) in albino Wistar rats. Twenty-five (25) rats were divided into five groups as follows: Group 1, the normal control, was maintained on standard rat chow and received normal saline (1 ml/kg body weight (BW)/day) for twelve weeks. The other groups were maintained on HFD for twelve weeks. Thereafter, groups 2–5 were treated with pioglitazone (4 mg/kg BW/day), RHB (0.6 ml/kg BW/day), normal saline (1 ml/kg BW/day), and fenofibrate (10 mg/kg BW/day), respectively. The animals were sacrificed after the experimental period. Biochemical indicators of oxidative stress and inflammation were assayed in the liver according to standard methods. The histological features of the liver were also compared to assess liver damage. RHB significantly (p<0.05) reduced body weight and liver index, inhibited oxidative stress, boosted antioxidant enzymes by increasing the activity and level of SOD and GSH, reduced proinflammatory markers (IL-2, IL-6, TNF-α), and reversed histological alterations induced by NAFLD in rat liver. In conclusion, the anti-inflammatory activity of RHB in the prevention of NAFLD in rats has been confirmed.

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Therapeutic effect of treatment with metformin and/or 4-hydroxychalcone in male Wistar rats with nonalcoholic fatty liver disease

European Journal of Pharmacology ◽

10.1016/j.ejphar.2019.172699 ◽

2019 ◽

Vol 863 ◽

pp. 172699 ◽

Cited By ~ 3

Author(s):

Selene de Jesús Acosta-Cota ◽

Elsa Maribel Aguilar-Medina ◽

Rosalío Ramos-Payán ◽

José Guadalupe Rendón Maldonado ◽

José Geovanni Romero-Quintana ◽

...

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

Therapeutic Effect ◽

Fatty Liver Disease ◽

Wistar Rats ◽

Nonalcoholic Fatty Liver ◽

Male Wistar Rats ◽

Effect Of Treatment

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Hepatoprotective effect of silymarin on fructose induced nonalcoholic fatty liver disease in male albino wistar rats

BMC Complementary Medicine and Therapies ◽

10.1186/s12906-021-03275-5 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Tewodros Mengesha ◽

N. Gnana Sekaran ◽

Tsegaye Mehare

Keyword(s):

Oxidative Stress ◽

Liver Disease ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

Fatty Liver Disease ◽

Wistar Rats ◽

Tap Water ◽

Control Group ◽

Hepatic Triglyceride ◽

Nonalcoholic Fatty Liver

Abstract Background Nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease in the Western world, and it’s likely to parallel the increasing prevalence of type 2 diabetes, obesity, and other components of metabolic syndrome. However, optimal treatment for NAFLD has not been established yet. Therefore, this study investigated the hepatoprotective effect of silymarin on fructose-induced nonalcoholic fatty liver disease in rats. Methods Thirty male Wistar rats were randomly divided into five groups; normal control group that consumed tap water, silymarin control group that consumed tap water and silymarin (400 mg/kg/day), fructose control group that consumed 20% fructose solution, treatment group that consumed 20% fructose solution and silymarin (200 mg/kg/day), and another treatment group that consumed 20% fructose solution and silymarin (400 mg/kg/day). Hepatic triglyceride, serum lipid profile, lipid peroxidation, antioxidant level, morphological features, and histopathological changes were investigated. The data were analyzed using one-way analysis of variance (ANOVA) followed by Tukey multiple comparison test. Statistical significance was determined at p < 0.05. Results This study showed that the fructose control group had a significantly high value in the stage of steatosis grade, hepatic triglyceride, serum triglyceride, total cholesterol, low-density lipoprotein cholesterol, alanine aminotransferase, aspartate aminotransferase, and hepatic malondialdehyde concentration as compared to the normal control. However, significantly low values of reduced glutathione and plasma total antioxidant capacity were found. The altered parameters due to fructose drastic effect were ameliorated by silymarin treatment. Conclusions The fructose control group developed dyslipidemia, oxidative stress, and mild steatosis that are the characteristics features of NAFLD. However, silymarin-treated groups showed amelioration in oxidative stress, dyslipidemia, and steatosis.

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Correction to: Hepatoprotective effect of silymarin on fructose induced nonalcoholic fatty liver disease in male albino wistar rats

BMC Complementary Medicine and Therapies ◽

10.1186/s12906-021-03313-2 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Tewodros Mengesha ◽

Natesan Gnanasekaran ◽

Tsegaye Mehare

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

Fatty Liver Disease ◽

Wistar Rats ◽

Hepatoprotective Effect ◽

Nonalcoholic Fatty Liver

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The role and possible mechanism of the long noncoding RNA LINC01260 in nonalcoholic fatty liver disease

Nutrition & Metabolism ◽

10.1186/s12986-021-00634-4 ◽

2022 ◽

Vol 19 (1) ◽

Author(s):

Xiaoxiao Ge ◽

Tao Sun ◽

Yanmei Zhang ◽

Yongqing Li ◽

Peng Gao ◽

...

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

Differential Expression ◽

Fatty Liver Disease ◽

Lipid Droplets ◽

Expression Profiles ◽

Nonalcoholic Fatty Liver ◽

Oil Red O Staining ◽

Oil Red O

Abstract Objective To investigate the differential expression profile of lncRNAs in the nonalcoholic fatty liver disease (NAFLD) model induced by oleic acid (OA) and to further explore the role of LINC01260 (ENST00000255183) in NAFLD, providing theoretical support for the clinical value of lncRNAs in NAFLD. Methods OA (50 μg/mL) was used to induce steatosis in normal human LO2 hepatocytes for 48 h and was verified by Oil red O staining. Differential expression profiles of lncRNAs were obtained by eukaryotic circular sequencing (RNA/lncRNA/circRNA-seq) techniques. A gain-of-function (GOF) strategy for LINC01260 was adopted, Oil red O staining and semiquantitative analysis were combined to explore whether the GOF of LINC01260 affects LO2 cell steatosis. CeRNA-based bioinformatics analysis of lncRNAs was performed, and the enriched mRNAs were further verified. RXRB siRNAs were applied and verify its role in LINC01260 regulated OA-induced hepatocytes steatosis. Results Lipid droplets of different sizes were observed in the cells of the OA group. Absorbance in the OA group was significantly increased after isopropanol decolorization (P < 0.05). Compared with those in the control group, there were 648 lncRNAs with differential expression greater than 1 time in the OA group, of which 351 were upregulated and 297 were downregulated. Fluorescence quantitative PCR showed that the expression of LINC01260 in the OA group was downregulated by 0.35 ± 0.07-fold (P < 0.05). The formation of lipid droplets in LO2 cells of the LINC01260 GOF group decreased significantly (P < 0.05). CeRNA analysis indicated that the mRNA levels of RXRB, RNPEPL1, CD82, MADD and KLC2 were changed to different degrees. Overexpression of LINC01260 significantly induced RXRB transcription (P < 0.05) and translation, and RXRB silence attenuated the lipids decrease induced by LINC01260 overexpression. Conclusion The OA-induced NAFLD cell model has a wide range of lncRNA differential expression profiles. LINC01260 participates in the regulation of the lipid droplet formation process of NAFLD, and its overexpression can significantly inhibit the steatosis process of LO2 cells. Mechanistically, LINC01260 may act as a ceRNA to regulate the expression of RXRB, thereby affecting the adipocytokine signaling pathway.

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