Zaied, K., Mohamed, H., Abd El-Twab, S., Abdul-Hamid, M. (2021). Ameliorative Effects of Panax Ginseng on Lung of Lambada Cyhalotherin-intoxicated Rats. Egyptian Journal of Histology, 44(1), 61-82. doi: 10.21608/ejh.2020.30560.1293
Karim Zaied; Hanaa Mohamed; Sanaa Abd El-Twab; Manal Abdul-Hamid. "Ameliorative Effects of Panax Ginseng on Lung of Lambada Cyhalotherin-intoxicated Rats". Egyptian Journal of Histology, 44, 1, 2021, 61-82. doi: 10.21608/ejh.2020.30560.1293
Zaied, K., Mohamed, H., Abd El-Twab, S., Abdul-Hamid, M. (2021). 'Ameliorative Effects of Panax Ginseng on Lung of Lambada Cyhalotherin-intoxicated Rats', Egyptian Journal of Histology, 44(1), pp. 61-82. doi: 10.21608/ejh.2020.30560.1293
Zaied, K., Mohamed, H., Abd El-Twab, S., Abdul-Hamid, M. Ameliorative Effects of Panax Ginseng on Lung of Lambada Cyhalotherin-intoxicated Rats. Egyptian Journal of Histology, 2021; 44(1): 61-82. doi: 10.21608/ejh.2020.30560.1293
Ameliorative Effects of Panax Ginseng on Lung of Lambada Cyhalotherin-intoxicated Rats
1Department of Zoology, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt
2Department of Zoology, Faculty of Science, Beni-Suef University, Egypt
Abstract
Introduction: Lambada-cyhalotherin (LCT) caused severe oxidative damage in liver, lung and testis. Aim of the Study: The objective of this research was to evaluate the ameliorative activity and underlying techniques of pure Panax ginseng (G) using rat model of LCT-induced lung damage. Materials and Methods: 36 male adult laboratory rats Rattus norvegicus domestica in weights around 135±10 g were separated into 6 experimental groups: 1st control group. 2nd and 3th groups were G groups (100 and 200 mg G/kg b. wt.) LCT group was given by oral gavage LCT (61.2 mg /kg b. wt.) that is equivalent to 1/10 of LD50. The 5th and 6th groups were co-treated with two doses of G. Results: LCT significantly decreased superoxide dismutase (SOD), catalase (CAT) and total thiol (T. thiol) and increased lipid peroxidation (LPO). mRNA and protein expression levels of p53 gene (apoptotic gene) were increased, whereas, Bcl-2 gene (anti-apoptotic gene) mRNA and protein expression levels were decreased in LCT-treated animals. Also, light microscopic and ultrastructure studies for lung tissues of LCT-treated animals showed marked hyperplasia of dilated bronchioles wall, RBCs extravasation in bronchiolium lumen and mononuclear leukocytic infiltration in parenchyma. Additionally, blood vessels congested with thickened walls, alveoli appeared collapsed with compensatory expansion of adjacent alveoli divided by thickened inter-alveolar septa, besides to damage in type 1 and type 2 pneumocytes. G co-treatment attenuated oxidative stress biomarkers. Both tested doses of G significantly decreased p53 and elevate Bcl-2 mRNA and protein expression levels and revealed significant amelioration and restoration of normal histology and ultrastructure of lung. Conclusion: In summary, G has exhibited ameliorative activity against oxidative stress induced by LCT in lung, apoptosis, histopathological and ultrastructural changes in albino rats.
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