ABSTRACT
Background: Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) are 2 common liver diseases that currently lack effective treatment options. Objectives: This study aimed to investigate the effect of lipopolysaccharide (LPS)-stimulated adipose-derived stem cells (ADSCs) on NAFLD treatment in an animal model. Methods: Male Wistar rats were fed a high-fat diet (HFD) to induce NAFLD for 7 weeks. The rats were then categorized into 3 groups: Mesenchymal stem cell (MSC), MSC + LPS, and fenofibrate (FENO) groups. Liver and body weight were measured, and the expression of genes involved in fatty acid biosynthesis, ß-oxidation, and inflammatory responses was assessed. Results: Lipopolysaccharide-stimulated ADSCs were more effective in regulating liver and body weight gain and reducing liver triglyceride (TG) levels compared to the other groups. Treatment with LPS-stimulated ADSCs effectively corrected liver enzymes, including alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and lipid factors, including low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) values, better than treatment with both FENO and MSCs. ADSCs + LPS treatment significantly decreased transforming growth factor ß (TGF-ß) and genes associated with inflammatory responses. Additionally, there was a significant reduction in reactive oxygen species (ROS) levels in the rats treated with ADSCs + LPS. Conclusions: Lipopolysaccharide-stimulated ADSCs showed potential in alleviating NAFLD by reducing inflammatory genes and ROS levels in HFD rats, demonstrating better results than treatment with ADSCs and FENO groups alone.
ABSTRACT
Background: In hepatic damage, Hepatic stellate cells (HSCs) become active, proliferate, and change to myofibroblasts. Increasing the fibrogenic genes, such as Transforming growth factor-ß (TGF-ß), Alpha Smooth Muscle Actin (α-SMA), and Collagen1 α (COL 1α) show that the activation of HSCs can lead to hepatic fibrosis. Purpose: These days people consume much cholesterol, palmitic acid, and glucose which can have adverse effects on an individuals' health, but their influences on activating human HSCs and inducing liver fibrosis have not been assessed. Our purpose is to investigate the effects of these three main and abundant ingredients in the diet on the activation of human HSCs and inducing liver fibrosis. Methods: To measure cholesterol, palmitic acid, and glucose cytotoxic effects on the viability of the cells, the MTT technique was used. Then the treated cells were incubated in media containing cholesterol, palmitic acid, and glucose with different concentrations for 24 h. At last, the α-SMA, COL 1α, and TGF-ß, genes mRNA expression were measured by real-time PCR. Results and Conclusions: Our results demonstrated that high concentrations of cholesterol and palmitic acid can activate human HSCs that lead to an increase in the mRNA expressions of fibrogenic genes. Thus, controlling fat intaking and knowing its mechanism is crucial to prevent and attenuate hepatic fibrosis.
ABSTRACT
PURPOSE: To evaluate the magnitudes and axis orientation of anterior corneal astigmatism (ACA) and posterior corneal astigmatism (PCA), the ratio of ACA to PCA, and the correlation between ACA and PCA in the different stages of keratoconus (KCN). METHODS: This retrospective case series comprised 161 eyes of 161 patients with KCN (104 men, 57 women; mean age, 22.35 ± 6.10 years). The participants were divided into four subgroups according to the Amsler-Krumeich classification. A Scheimpflug imaging system was used to measure the magnitude and axis orientation of ACA and PCA. The posterior-anterior corneal astigmatism ratio was also calculated. The results were compared among different subgroups. RESULTS: The average amounts of anterior, posterior, and total corneal astigmatism were 4.08 ± 2.21 diopters (D), 0.86 ± 0.46 D, and 3.50 ± 1.94 D, respectively. With-the-rule, against-the-rule, and oblique astigmatisms of the posterior surface of the cornea were found in 61 eyes (37.9%), 67 eyes (41.6%), and 33 eyes (20.5%), respectively; corresponding figures in the anterior corneal surface were 55 eyes (32.4%), 56 eyes (34.8%), and 50 eyes (31.1%), respectively. A strong correlation (P ≤ 0.001, r = 0.839) was found between ACA and PCA in the different stages of KCN; the correlation was weaker in eyes with grade 3 (P ≤ 0.001, r = 0.711) and grade 4 (P ≤ 0.001, r = 0.717) KCN. The maximum posterior-anterior corneal astigmatism ratio (PCA/ACA, 0.246) was found in patients with stage 1 KCN. CONCLUSION: Corneal astigmatism in anterior surface was more affected than posterior surface by increasing in the KCN severity, although PCA was more affected than ACA in an early stage of KCN.
