scholarly journals Anti-inflammatory Mechanism of Ruzu Bitters on Diet-Induced Nonalcoholic Fatty Liver Disease in Male Wistar Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Olubanke O. Ogunlana ◽  
Oluseyi E. Ogunlana ◽  
Tobi S. Adekunbi ◽  
Babatunde O. Adetuyi ◽  
Bose E. Adegboye ◽  
...  

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.

2014 ◽  
Vol 307 (1) ◽  
pp. R26-R34 ◽  
Author(s):  
Maria Z. Alfaradhi ◽  
Denise S. Fernandez-Twinn ◽  
Malgorzata S. Martin-Gronert ◽  
Barbara Musial ◽  
Abigail Fowden ◽  
...  

Changes in the maternal nutritional environment during fetal development can influence offspring's metabolic risk in later life. Animal models have demonstrated that offspring of diet-induced obese dams develop metabolic complications, including nonalcoholic fatty liver disease. In this study we investigated the mechanisms in young offspring that lead to the development of nonalcoholic fatty liver disease (NAFLD). Female offspring of C57BL/6J dams fed either a control or obesogenic diet were studied at 8 wk of age. We investigated the roles of oxidative stress and lipid metabolism in contributing to fatty liver in offspring. There were no differences in body weight or adiposity at 8 wk of age; however, offspring of obese dams were hyperinsulinemic. Oxidative damage markers were significantly increased in their livers, with reduced levels of the antioxidant enzyme glutathione peroxidase-1. Mitochondrial complex I and II activities were elevated, while levels of mitochondrial cytochrome c were significantly reduced and glutamate dehydrogenase was significantly increased, suggesting mitochondrial dysfunction. Offspring of obese dams also had significantly greater hepatic lipid content, associated with increased levels of PPARγ and reduced triglyceride lipase. Liver glycogen and protein content were concomitantly reduced in offspring of obese dams. In conclusion, offspring of diet-induced obese dams have disrupted liver metabolism and develop NAFLD prior to any differences in body weight or body composition. Oxidative stress may play a mechanistic role in the progression of fatty liver in these offspring.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Tewodros Mengesha ◽  
N. Gnana Sekaran ◽  
Tsegaye Mehare

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.


2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Po-Jung Wu ◽  
Jin-Bor Chen ◽  
Wen-Chin Lee ◽  
Hwee-Yeong Ng ◽  
Shu-Ching Lien ◽  
...  

Introduction. Nonalcoholic fatty liver disease (NAFLD) is becoming more common around the world and it may progress to cirrhosis and liver failure, increasing mortality risk. In hemodialysis (HD) patients, NAFLD may be a novel risk factor for their high cardiovascular mortality. Heightened oxidative stress is highly prevalent in HD patients. However, the relationship between oxidative stress and NAFLD in HD patients is not well defined.Methods. We studied seventy-one stable nondiabetic HD patients. Nineteen patients had the diagnosis of NAFLD by ultrasonography. Blood levels of oxidative stress markers were measured in each patient, including thiobarbituric acid reactive substances (TBARS), free thiols, superoxide dismutase (SOD) activities, and glutathione peroxidase (GPx) activity. The copy numbers of mitochondrial DNA (mtDNA) in peripheral leukocytes were also determined. Demographic, biochemistry, and hemogram data were recorded. The two groups of patients were compared in order to determine the factors associated with NAFLD in HD patients.Findings. Compared to those without NAFLD, nondiabetic HD patients with NAFLD had significantly higher mtDNA copy number and GPx levels. The two groups did not differ significantly in dialysis adequacy, hemoglobin, serum calcium, phosphorus, albumin, liver function tests, or lipid profiles. Regression analysis confirmed mtDNA copy numbers and GPx levels as two independent factors associated with NAFLD. Compared to those with polysulfone, patients dialyzed with cellulose membrane have significantly higher levels of TBARS. However, patients with or without NAFLD did not differ in their use of either dialysis membrane.Discussion. Oxidative stress (represented by antioxidant defense, GPx) and mitochondrial DNA copy numbers are independently associated with fatty liver disease in nondiabetic HD patients. The diagnostic and therapeutic implications of this key observation warrant further exploration.


2019 ◽  
Vol 25 (11) ◽  
pp. e146-e147 ◽  
Author(s):  
Mitsuro Chiba ◽  
Kunio Nakane ◽  
Hitoshi Abe ◽  
Masafumi Komatsu ◽  
Haruhiko Tozawa

Abstract Nonalcoholic fatty liver disease (NAFLD) develops in ulcerative colitis (UC) and Crohn’s disease. However, there is scarce reporting on the onset of UC in patients with NAFLD. A 44-year-old man was diagnosed with UC and referred to us in 2019. His height was 166.0 cm, and body weight was 86.3 kg. The waist circumference was 93.7 cm (normal range <85) and triglyceride was 751 mg/dL. These findings, in addition to hypertension, resulted in a diagnosis of metabolic syndrome. HbA1c was normal. Ultrasonography disclosed severe fatty liver. Nonalcoholic fatty liver disease was diagnosed. He underwent 12 days of educational hospitalization for UC. A lacto-ovo-semi-vegetarian diet (1400 kcal/day), a kind of plant-based diet (PBD), was provided. He lost 4 kg, which was 4.6% of his base body weight. Triglyceride and total cholesterol decreased to the normal ranges. Transaminases and γ-glutamyl transpeptidase also decreased. His body weight decreased further after discharge. Follow-up ultrasonography indicated an improvement in hepatic enlargement. The shear wave velocity decreased from 1.11 to 0.88 m/s. His soft stool became normal stool by 2 months after discharge. Records of his health checkups revealed the presence of metabolic syndrome and abnormal liver function tests already in 2015. Thus, it was concluded that UC developed in a patient with NAFLD in this case. Plant-based diet has already been shown to be effective in inflammatory bowel disease (IBD). In the present case, NAFLD parameters were dramatically improved by PBD. Whether the improvement was due to weight loss per se or due to weight loss with PBD is to be clarified.


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