Data Highlights the Ameliorative Effects of Nigella sativa, Atorvastatin, or L-carnitine on HFD-Caused Detriments in Male Albino Rats
Description
The data of this study was aimed to investigate the effect of 4 weeks high fat diet (HFD) administration to male albino rats and putative alleviation potentials of Nigella sativa, atorvastatin, or L-carnitine administered in the last 2 weeks of the experiment in doses of 300 mg/kg/day, 5 mg/kg/day, or 200 mg/kg/day respectively. Screening of serum atherogenic index (AX) was done after 2 weeks of starting the experiment according to formula: log10 (TG/HDL-c). Rats exhibited AX less than 0.24 were excluded. Rats with AX more than 0.24 were allocated into the HFD group and the other 3 treated groups (as shown in table 1 and fig. 1) for supplementing the tested materials. At the end of the experiment, blood samples were collected and the rats were killed by sudden cervical decapitation while they were anaesthetized. Serum ALT, AST, ALP, and GGT activities beside atherogenic index were estimated. Histological examination Samples of hepatic tissues from control and treated rats were collected and fixed in PFA 4 % and then embedded in paraffin wax and processed using routine hematoxylin and eosin staining (H&E). Then, sections were examined under a light microscope. Results Histological examination of liver of control group showed the typical normal histological structure of hepatic parenchyma (Fig. 2). Livers of rats fed on HFD revealed swollen hepatocytes with marked to severe steatosis characterized mainly by lipid deposition which appear as clear vacuoles. Moreover, pericentral coagulative necrosis, as well as scattered inflammatory cell infiltration, were also observed (Fig. 3). Histological examination of the livers of NS-received group showed significantly moderated hepatic steatosis. (Fig. 4 and 5). Histologic examination of atorvastatin-received rats; the liver showed mild degenerated changes in hepatocytes and a definite improvement in the hepatic architecture compared to the HFD group. The lipid droplet diameter, the number of lipid droplets, and area covered by the lipid droplets were significantly lowered (Fig. 6 and 7). LC-received group; the liver showed that hepatocytes had normal-sized nuclei, the number and the size of vacuoles were markedly decreased, the cell boundaries were clear. Central veins, blood vessels of the portal triad, and the hepatic sinusoids are congested and engorged with blood (Fig. 8 and 9). Conclusion Although HFD raised significantly serum atherogenic index by 31% relative to normal control’s one, both NS and atorvastatin ameliorated, separately, this effect which was confirmed by histopathological examination of hepatic tissues. On the other side, LC decreased insignificantly the raised atherogenic index by a condition of our study (table 10). Nevertheless, the tested materials did not, at least, worsen the liver function indices (table 4 and 10)), but ameliorate the hepatic histological architecture, which confirm the safety of tested materials for treating HFD-induced dyslipidemia in rats.