Health benefits of sesamin on cardiovascular disease and its associated risk factors

Abstract

Sesamin, a major lignin isolated from sesame (Sesamum indicum) seeds and sesame oil, is known to possess antioxidant and anti-inflammatory properties. Several studies have revealed that oxidative stress and inflammation play a major role in a variety of cardiovascular diseases (CVDs). This comprehensive review summarizes the evidence on the effects of sesamin on CVD and its risk factors, principally due to its antioxidant properties. Specifically, this review highlights the mechanisms underlying the anti-hypertensive, anti-atherogenic, anti-thrombotic, anti-diabetic, and anti-obesity, lipolytic effects of sesamin both in vivo and in vitro, and identifies the signaling pathways targeted by sesamin and its metabolites. The data indicates that RAS/MAPK, PI3K/AKT, ERK1/2, p38, p53, IL-6, TNFα, and NF-κB signaling networks are all involved in moderating the various effects of sesamin on CVD and its risk factors. In conclusion, the experimental evidence suggesting that sesamin can reduce CVD risk is convincing. Thus, sesamin can be potentially useful as an adjuvant therapeutic agent to combat CVD and its multitude of risk factors.

Keywords: Atherosclerosis; CVD; Diabetes; Hypertension; Obesity; Sesamin; Thrombosis.

Fig. 1

The mechanism of action by which sesamin enhances NO bioactivity in the aortas of spontaneously hypertensive rats (SHR). The sesamin-mediated suppression of eNOS uncoupling, via regulation of DHFR and ONOO- levels, coupled with the stimulatory effect of sesamin on p-eNOS increases NO biosynthesis to relieve endothelial dysfunction and hypertension. Sesamin also inhibits NADPH oxidase, subsequently decreasing superoxide levels and NO oxidative inactivation, contributing to the suppression of endothelial dysfunction and hypertension (adapted from Kong et al., 2015a).

Fig. 2

The mechanism of action underlying the anti-proliferative action of sesamin on PDGF-induced VSMCs. Sesamin upregulates p53, leading to the upregulation of p21 and eventually p27. This leads to the suppression of cyclin D1, cyclin E, CDK2, and CDK4. In turn, the levels of PCNA and p-pRb are reduced, inhibiting VSMC proliferation (adapted from Han et al., 2015).

Fig. 3

A summary of the main regulatory effects of sesamin on proteins and signaling factors involved in hypertension, atherosclerosis, thrombosis, diabetes, and obesity. The upward-pointing arrows indicate positive regulation, while downward-pointing arrows indicate negative regulation.