Impact of β-alanyl-L-histidine against HypercholesterolemiaSanaa A Ali*, Manal A Hamed, and Nagy Saba El Rigal
Therapeutic Chemistry Department, National Research Center, Dokki, Cairo, Egypt.
- *Corresponding Author:
- Sanaa A Ali
Therapeutic Chemistry Department, National Research Center, Dokki, Cairo, Egypt
Received date: 23 October 2012 Accepted date: 01 May 2013
β-alanyl-L-histidine, an endogenous histidine-containing dipeptide, protects protein from oxidation and glycation, which may contribute to a potential treatment for some conformational diseases including cataract. The effect of hypercholesterolemia in rabbits was tested on serum protein fractions, lactate dehydrogenase isoenzymes, total protein and glucose levels. The work was extended to estimate certain hepatic enzymes; glucose-6- phosphatase (G-6-Pase), glycogen phosphorylase (GPH), α-hydroxybutyrate dehydrogenase (α-HBDH), lactate dehydrogenase (LDH) and glycogen content. The corrective action of β-alanyl-L-histidine (carnosine) and fluvastatin were also evaluated. Twenty five adult male Newzeland rabbits were selected for this study. The animals were divided into five groups. Group 1 served as normal healthy control, group 2; hypercholesterolemic animals (fed on standard rabbit’s chow with 1% cholesterol for 12 weeks), group 3; high carnosine dose (50 mg/Kg b. wt.) treated animals, group 4; low carnosine dose ( 25 mg/Kg b. wt.) treated ones and group 5; fluvastatin (2mg/kg b.wt.) treated group. Treatment started at the last six weeks of cholesterol feeding. Hypercholesterolemic rabbits recorded drastic changes in all parameters under investigation. β-alanyl-L-histidine has been demonstrated to provide protection against oxidative damage with respect to fluvastatin. β-alanyl-L-histidine and fluvastatin recorded an enhancement level in major parameters, where high carnosine dose recorded the most potent effect.