Role of C-Reactive
Protein in the Development of Atherosclerosis in
Diet-induced Lipidemia in Albino Rats
RP Kalsait1, PB Khedekar2, AN
Saoji2 and KP Bhusari1
1Sharad
Pawar College of Pharmacy, Wanadongri, Hingna Road,
Nagpur – 441 110, 2University
Department of Pharmaceutical Sciences, Amravati Road,
Nagpur, India
*For correspondence:
E-mail:
kalsait.ravi@gmail.com
Tel:
(07104) 236352, 9960099852; Fax: (07104) 235084
Received: 2 July
2010 Revised
accepted: 12 December 2011
Tropical
Journal of Pharmaceutical Research, February 2011;
10(1):
41-45
Abstract
Purpose:
Blood C-reactive protein level serves as a useful
biomarker of generalized injury and inflammation. Vast
amounts of clinical data suggest its serum level
predicts risk of cardiovascular disease. In the present
study, the role of C-reactive protein in the development
of atherosclerosis in albino rats was investigated.
Methods: Wistar
breed albino rats were divided into two groups. Group I
was fed on normal pellet diet while group II fed on high
fat diet for up to 120 days, and blood serum was
analyzed for C-reactive protein and lipid profile. Lipid
profile included determination of total cholesterol, HDL
cholesterol, LDL cholesterol, and triglycerides. After
sacrifice of the animals, the heart and aorta were
removed for histopathological studies.
Results:
The concentration of C-reactive protein did not increase
in group II but a significant increase in lipid profile
was observed (p < 0.001). In histopathological studies,
sections of the aorta showed lesions in tunica intima;
the branch of coronary artery showed lipid infiltration
in its wall while myocardial infarct was clearly
observed in the myocardium.
Conclusion:
Feeding the rats high fat diet for 120 days did not
increase C-reactive protein level but significant
increases in lipid levels were observed in group II.
These data indicate that in albino rats, C-reactive
protein does not play any role in the development of
atherosclerosis.
Keywords:
C-reactive protein, Hyperlipidemia, Coronary Heart
Disease
