Objective: To investigate whether hydro-alcoholic extract of aerial parts of (CFE) could attenuate high-fat diet (HFD) induced cardiac damage.

Methods: Forty rats were divided into five groups: control (C), treated with CFE, treated with HFD, HFD treated with CFE, and HFD treated with metformin (Met).

Results: CFE treatment significantly ( < .001) attenuated HFD-induced increase in cardiac lipids such as total lipids, triglycerides, total cholesterol, and free fatty acids and decreased phospholipids accompanied by increasing in lipid peroxidation and protein oxidation. Furthermore, significant reduction in the activities of antioxidant enzymes, creatine kinase and aldose reductase and sorbitol dehydrogenase was also observed in HFD fed rats. These changes were alleviated by CFE. Moreover, the histopathological observations of heart are also in agreement with the biochemical findings.

Conclusion: The present study confirmed that CFE could be used as adjuvant therapy for preventing or managing high fat diet induced cardiac damage.

Download full-text PDF

Source
http://dx.doi.org/10.1080/13813455.2019.1693601DOI Listing

Publication Analysis

Top Keywords

high-fat diet
8
treated cfe
8
hfd treated
8
preventive high-fat
4
diet induced
4
induced injury
4
injury heart
4
heart modulation
4
modulation tissue
4
tissue lipids
4

Similar Publications

This study aimed to investigate the effects of heat-killed N1 (HK-N1) and lipoteichoic acid (LTA) derived from it on alleviating insulin resistance by modulating the gut microbiota and amino acid metabolism. High-fat diet (HFD)-fed mice were administered live bacteria or HK-N1, and the results demonstrated that HK-N1 significantly reduced epididymal adipocyte size and serum low density lipoprotein-cholesterol, and improved insulin resistance by increasing the YY peptide and glucagon-like peptide levels. HK-N1 also modulated the gut microbiome composition, enhancing microbiota uniformity and reducing the abundance of , and .

View Article and Find Full Text PDF

polysaccharides alleviate metabolic dysfunction-associated steatotic liver disease through enhancing hepatocyte RelA/ HNF1α signaling.

World J Gastroenterol

January 2025

State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Key Laboratory of Molecular Biology for Endemic Diseases, Department of Pathology, School of Basic Medical Sciences, Xinjiang Medical University, Urumqi 830000, Xinjiang Uyghur Autonomous Region, China.

Background: polysaccharides (BSP) have antioxidant, immune regulation, and anti-fibrotic activities. However, the therapeutic effect and mechanisms underlying the action of BSP in metabolic dysfunction-associated steatotic liver disease (MASLD) have not been fully understood.

Aim: To investigate the therapeutic effects and mechanisms of BSP on MASLD by centering on the hepatocyte nuclear factor kappa B p65 (RelA)/hepatocyte nuclear factor-1 alpha (HNF1α) signaling.

View Article and Find Full Text PDF

Objectives: This study aimed to evaluate the effects of pre-conditioning exercise on body lipid metabolism, leptin secretion, and the downstream pathways at the early stage of type 2 diabetes mellitus (T2DM).

Materials And Methods: The T2DM model was established using an 8-week high-sugar, high-fat diet combined. The T2DM model was established using an 8-week high-sugar, high-fat diet combined with streptozocin (STZ) injection.

View Article and Find Full Text PDF

Unraveling the pathophysiology of type 2 diabetes with a new selectively bred animal model, the Oikawa-Nagao mouse.

Diabetol Int

January 2025

Department of Endocrinology, Metabolism and Nephrology, Graduate School of Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-Ku, Tokyo, 113-8603 Japan.

Type 2 diabetes (T2D) is a polygenic disease, and the development of animal models by selective breeding is crucial for understanding its etiology, pathophysiology, complications, and treatments. We recently developed a new T2D model, the Oikawa-Nagao (ON) mouse, by selectively breeding mice with inferior glucose tolerance [diabetes-prone (ON mouse DP®; ON-DP) strain] and superior glucose tolerance [diabetes-resistant (ON mouse DR®; ON-DR) strain] on a high-fat diet. ON-DP mice are predisposed to develop diabetes and obesity after being fed a high-fat diet, compared to ON-DR mice.

View Article and Find Full Text PDF

Background: Sorafenib, an FDA-approved drug for advanced hepatocellular carcinoma (HCC), faces resistance issues, partly due to myeloid-derived suppressor cells (MDSCs) that enhance immunosuppression in the tumor microenvironment (TME).

Methods: Various murine HCC cell lines and MDSCs were used in a series of in vitro and in vivo experiments. These included subcutaneous tumor models, cell viability assays, flow cytometry, immunohistochemistry, and RNA sequencing.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!