Investigation of cardioprotective effects of Leea rubra Blume leaves on isoproterenol-induced left ventricular hypertrophy in mice
سال انتشار: 1405
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 1
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شناسه ملی سند علمی:
JR_HERM-15-1_003
تاریخ نمایه سازی: 23 دی 1404
چکیده مقاله:
Introduction: Cardiac hypertrophy is a risk factor for many cardiovascular diseases (CVDs). Species of the genus Leea have traditional cardioprotective uses, but their direct effects on the heart remain unreported. This study evaluated the cardioprotective activities of a crude methanolic extract (CME) of L. rubra leaves (LRL) in isoproterenol-induced cardiac hypertrophic mice (IIHM) using atorvastatin as a reference treatment. Methods: IIHM (induced with isoproterenol, ۵ mg/kg, ۷ days, intraperitoneally) were treated with CME of LRL (۴۰ mg/kg or ۸۰ mg/kg, ۲۸ days, orally) and compared with a standard treatment group (atorvastatin, ۲۰ mg/kg, ۲۸ days, orally) and a negative control group (IIHM, placebo). The cardioprotective and hepatoprotective effects of the extract were evaluated by analysing the changes in blood biochemical parameters, including lipid profile (total cholesterol [TC], triglyceride [TG], high-density lipoprotein [HDL], and low-density lipoprotein [LDL]), cardiac troponin I (CTnI), serum glutamic pyruvic transaminase (SGPT), and serum glutamic oxaloacetic transaminase (SGOT). Analysis was conducted using various commercial test kits. The left ventricular weight and body weight (LVW/BW) ratio was also recorded. Results: LRL significantly improved the lipid profile by lowering TC, TG, and LDL while increasing HDL levels (P<۰.۰۰۰۱). Significant cardioprotective (reduced serum CTnI level and LVW/BW ratio (P<۰.۰۰۰۱)) and hepatoprotective (reduced serum SGPT and SGOT levels (P<۰.۰۰۰۱)) activities were observed in IIHM compared with the negative control group. Conclusion: The present study found antihyperlipidemic, cardioprotective, and hepatoprotective activity after LRL treatment in IIHM. Further investigation is required to identify the compounds and molecular mechanisms responsible for these effects.