Evaluation of Serotonin Modular in Chemically Induced Ischemic Stroke and Associated Cachexia

Abstract

Aim and objective: Cachexia is a multifactorial syndrome characterized by an ongoing loss of skeletal muscle mass with loss of fat mass, and progressive functional impairment which cannot be fully reversed by conventional nutrition support. One group of researchers found that the prevalence of cachexia is 21% in 1 year of subsequently stroke. Cachexia is energy wasting syndrome that causes skeletal muscle wasting and skeletal muscle atrophy. Inflammatory markers are increased in ischemic stroke, which leads to cachexia and skeletal muscle protein breakdown. No research is available of serotonin modulator in stroke cachexia. The objective of the study is to evaluate the effect of SSRI on stroke cachexia. To develop a therapeutic strategy for stroke cachexia. Material and method: The study was carried out using endothelin-1 (ET-1) induce stroke cachexia model. For this study we used six to ten weeks old male and female wistar rats. Induction of ischemic stroke was done with 3 μl of 80 μM ET1 was infused at a rate of 1 μl per min. Buspirone was administered at dose 3mg/kg for 28 days. Parameters were evaluated body mass marker, markers of carbohydrate metabolism, markers of lipid metabolism, inflammatory markers, and skeletal muscle wasting markers. Result: The animals treated with buspirone significantly decrease in glucose, TNF-α, IL-6 level as compared to disease control animals. Treatment with buspirone significantly increases in body weight, food intake, lipids levels, and fats. Conclusion: Our data suggest that buspirone produces a beneficial effect on stroke cachexia. Buspirone was successful to reduce the levels of inflammatory cytokines, ameliorate the effects on stroke-induce skeletal muscle wasting, lipid levels, fat levels, and carbohydrate metabolism.