S-Allylcysteine Attenuates Myocardial Injury Via Antioxidant Pathway in Ovariectomised Rat Model

Read the full article See related articles

Listed in

This article is not in any list yet, why not save it to one of your lists.
Log in to save this article

Abstract

Cardiovascular disease is the primary cause of death in Malaysia, with post-menopausal women at higher risk due to oestrogen deficiency. Consequently, researchers are exploring alternative approaches to minimize cardiovascular injury in post-menopausal women. S-Allylcysteine (SAC), a compound in aged garlic extract has demonstrated cardioprotective effects through mitochondrial preservation and the CSE/hydrogen sulfide (H 2 S) pathway. This study investigated the impact of SAC in ovariectomised rats with isoprenaline-induced myocardial injury. Ovariectomy surgery was performed on 32 female Wistar rats, while eight rats underwent sham surgery. After three weeks, all rats received subcutaneous administration of either normal saline (Sham OVX) or isoprenaline 85 mg/kg (OVXM) for two days to induce myocardial injury. Then distilled water (Sham, OVX, OVXM) or SAC 100 mg/kg (OVXS, OVXMS) were orally given for one week. Blood pressure was monitored before and after treatment and cardiac function was measured using Langendorff’s system after treatment. Structural changes and fibrosis of the heart were assessed by histological analysis. Biochemical analysis were conducted using colorimetric methods and Western blot for protein expression. Histological observation indicated that SAC limit hypertrophy and collagen deposition in the OVXMS group. Although SAC did not reduce TBARS levels, it increased GSH and SOD antioxidants levels. CSE enzyme activity and protein expression showed a trend of increment in SAC-treated group. In summary, this study demonstrates SAC's potential in preserving cardiac function and structure under oestrogen-deficient conditions. However, further in-depth study is warranted to understand the antioxidant and CSE enzyme signalling pathways.

Article activity feed