Heart failure-associated morbidity and mortality is largely attributable to extensive and unregulated cardiac remodelling. Roselle (Hibiscus sabdariffa) calyces are enriched with natural polyphenols known for antioxidant and anti-hypertensive effects, yet its effects on early cardiac remodelling in post myocardial infarction (MI) setting are still unclear. Thus, the aim of this study was to investigate the actions of roselle extract on cardiac remodelling in rat model of MI. Male Wistar rats (200-300 g) were randomly allotted into three groups: Control, MI, and MI + Roselle. MI was induced with isoprenaline (ISO) (85 mg/kg, s.c) for two consecutive days followed by roselle treatment (100 mg/kg, orally) for 7 days. Isoprenaline administration showed changes in heart weight to body weight (HW/BW) ratio. MI was especially evident by the elevated cardiac injury marker, troponin-T, and histological observation. Upregulation of plasma levels and cardiac gene expression levels of inflammatory cytokines such as interleukin (IL)-6 and IL-10 was seen in MI rats. A relatively high percentage of fibrosis was observed in rat heart tissues with over-expression of collagen (Col)-1 and Col-3 genes following isoprenaline-induced MI. On top of that, cardiomyocyte areas were larger in heart tissues of MI rats with upregulation of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) gene expression, indicating cardiac hypertrophy. Interestingly, roselle supplementation attenuated elevation of plasma troponin-T, IL-6, IL10, and gene expression level of IL-10. Furthermore, reduction of cardiac fibrosis and hypertrophy were observed. In conclusion, roselle treatment was able to limit early cardiac remodelling in MI rat model by alleviating inflammation, fibrosis, and hypertrophy; hence, the potential application of roselle in early adjunctive treatment to prevent heart failure.

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Myocardial infarction (MI)-associated inflammation is crucial for post-infarct healing. However, unregulated inflammation may lead to unnecessary systemic inflammation, and affect other organs. This study investigated the effects of MI on spleen and kidneys over early time-points (2 and 7 days) in isoprenaline-induced MI rat model. MI was evident by elevated levels of cardiac injury marker, troponin T, and lactate dehydrogenase (LDH). MI rats showed significant upregulation of myeloperoxidase (MPO) activity at day-2 post infarct while kidney MPO activity remained unaffected. Kidney function test revealed only slightly increased plasma urea at day-2 post MI with no changes in plasma creatine at both time-points. Histological observation on the spleen showed disorganization of spleen structure at day-2 post MI while the kidney structures were preserved at both time-points. In conclusion, although MI-associated damages in the spleen were seen at day-2 post infarct, it had no impact on the kidney structures at both time-points.