Aegeline mitigates isoproterenol-induced myocardial infarction: insights from biochemical, histopathological, and in silico studies

Figures

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  Figure 1. Effects of aegeline on body weight in experimental rats. (A) Body weight before treatment and (B) body weight after treatment. Data are presented as mean ± SEM (n = 6). Statistical significance was determined using one-way ANOVA followed by Tukey’s post hoc test. #P < 0.05 vs. the control group.

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  Figure 2. (A–D) Effects of aegeline on cardiac injury biomarkers in isoproterenol-induced myocardial infarction. (A) Cardiac troponin T (cTnT), (B) cardiac troponin I (cTnI), (C) creatine kinase-MB (CK-MB), and (D) lactate dehydrogenase (LDH). Data are presented as mean ± SEM (n = 6). Statistical significance was determined using one-way ANOVA followed by Tukey’s post hoc test. #P < 0.05 vs. the control group; *P < 0.05 and **P < 0.01 vs. the ISO group.

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  Figure 3. Effects of aegeline on neurohormonal markers in isoproterenol-induced myocardial infarction. (A) Aldosterone and (B) cortisol levels. Data are presented as mean ± SEM (n = 6). Statistical significance was determined using one-way ANOVA followed by Tukey’s post hoc test. #P < 0.05 vs. the control group; *P < 0.05 and **P < 0.01 vs. the ISO group.

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  Figure 4. Effects of aegeline on antioxidant status, oxidative stress, and nitrosative stress markers in isoproterenol-induced myocardial infarction. (A) Reduced glutathione (GSH), (B) catalase (CAT), (C) malondialdehyde (MDA), (D) reactive oxygen species (ROS), and (E) total nitrite/nitrate (NOx). Data are presented as mean ± SEM (n = 6). Statistical significance was determined using one-way ANOVA followed by Tukey’s post hoc test. #P < 0.05 vs. the control group; *P < 0.05 and **P < 0.01 vs. the ISO group.

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  Figure 5. Effects of aegeline on inflammatory mediators in isoproterenol-induced myocardial infarction. (A) Interleukin-1β (IL-1β), (B) interleukin-6 (IL-6), (C) tumor necrosis factor-α (TNF-α), and (D) nuclear factor kappa B (NF-κB). Data are presented as mean ± SEM (n = 6). Statistical significance was determined using one-way ANOVA followed by Tukey’s post hoc test. #P < 0.05 vs. the control group; *P < 0.05 and **P < 0.01 vs. the ISO group.

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  Figure 6. Effects of aegeline on hepatic and renal function markers in isoproterenol-induced myocardial infarction. (A) Aspartate aminotransferase (AST), (B) alanine aminotransferase (ALT), (C) urea, and (D) creatinine. Data are presented as mean ± SEM (n = 6). Statistical significance was determined using one-way ANOVA followed by Tukey’s post hoc test. #P < 0.05 vs. the control group; *P < 0.05 and **P < 0.01 vs. the ISO group.

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  Figure 7. Effects of aegeline on caspase-3 levels in isoproterenol-induced myocardial infarction. Caspase-3 levels were significantly increased in the ISO group compared with the control group, indicating enhanced apoptotic activity following myocardial injury. Treatment with aegeline at doses of 5 and 10 mg/kg significantly reduced caspase-3 levels compared with the ISO group. Data are presented as mean ± SEM (n = 6). Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. #P < 0.05 vs. control; *P < 0.05 and **P < 0.01 vs. ISO.

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  Figure 8. Effects of aegeline on myocardial histopathological alterations in isoproterenol-induced myocardial infarction. Representative hematoxylin and eosin (H&E)-stained myocardial sections (200× magnification; scale bar = 100 μm). (A) Control group showing normal myocardial architecture with well-organized cardiac muscle fibers, intact cytoplasmic striations, and uniformly distributed nuclei. (B) ISO-induced myocardial infarction group showing marked myocardial injury characterized by endocardial edema, myofibrillar degeneration, and extensive mononuclear inflammatory cell infiltration (black arrows). (C) ISO + aegeline (5 mg/kg) group showing partial preservation of myocardial architecture with moderate inflammatory cell infiltration and reduced tissue damage (green arrows). (D) ISO + aegeline (10 mg/kg) group showing near-normal myocardial morphology with minimal inflammatory cell infiltration and preserved myocardial fibers (green arrow). (E) Quantitative histopathological injury scores were determined using a blinded semiquantitative scoring system (0–4 scale). Data are presented as mean ± SEM (n = 6). Statistical analysis was performed using one-way ANOVA followed by Tukey’s post…

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  Figure 9. Two-dimensional and three-dimensional molecular interactions of the ligand aegeline with 3B6R, 7DBJ, 1J1D, and 7SC2.