Abstract Title:

Ameliorative effects of hempseed (Cannabis sativa) against hypercholesterolemia associated cardiovascular changes.

Abstract Source:

Nutr Metab Cardiovasc Dis. 2019 Sep 13. Epub 2019 Sep 13. PMID: 31668458

Abstract Author(s):

Naveen Kaushal, Shallu Dhadwal, Parminder Kaur

Article Affiliation:

Naveen Kaushal


BACKGROUND AND AIM: Hypercholesterolemia (HC) is a major risk factor for cardiovascular (CV) diseases, that are the major cause of mortality worldwide. Free radicals mediated oxidative stress is a critical player in HC-associated pathophysiological insults including atherosclerosis. Unwanted side effects associated with statins, COX-2 inhibitors, and other synthetic drugs limit their use. Thus, modulation of oxidative stress during HC using green pharmaceuticals seems an appropriate approach against deleterious CV consequences without noticeable side-effect. In this regard, owing to an abundance of proteins, fiber and optimal ratios of omega 6 PUFA: omega-3 PUFA in Hempseed (HS), we aim to exploit its anti-inflammatory and antioxidant properties to ameliorate HC- associated CV effects.

METHODS AND RESULTS: Comparing the antioxidant capacity of protein and lipid fractions of HS using ABTS and DPPH assays, HS was supplemented to high-fat diets (HFD) induced hypercholesterolemic wistar rats. After treatment schedules, lipid profiles, histological and ultrastructural investigations, gene and protein expressions of inflammatory markers, markers of oxidative stress were studied and correlated with biophysical parameters such as ECG and impedance/conductance across the aorta. HS demonstrating in vitro free radical scavenging activity, ameliorated the signs of HC as seen with improved lipid profiles, aortic tissue damage and ECG patterns compared to HFD groups. HS administration also relieved the COX-2 mediated inflammation, which correlated well with the improved redox status in the tissue.

CONCLUSIONS: Current study evidently demonstrates that the anti-hypercholesterolemic effects of HS are mediated through redox-sensitive modulation of inflammatory pathways.

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