Biological and physical studies on the protective and therapeutic roles of ashwagandha seed extract against the potential toxic effect of amoxicillin in rats

Author:

Aboelhassan Dalia M.1,Ibrahim Noha E.2,Elnasharty Mohamed M.M.3,Elwan Azhar M.4,Elhadidy Mohamed E.5,Mohamed Mona A.6,Radwan Hasnaa A.1,Ghaly Inas S.1,Farag Ibrahim M.1

Affiliation:

1. Department of Cell Biology, Biotechnology Research Institute, National Research Centre (NRC), 33 El Buhouth St, Dokki, Giza, 12622, Egypt

2. Department of Microbial Biotechnology, Biotechnology Research Institute, National Research Centre (NRC), 33 El Buhouth St, Dokki, Giza, 12622, Egypt

3. Department of Microwave Physics and Dielectrics, Physics Research Institute, National Research Centre (NRC), 33 El Bohouth st., Dokki, Giza, 12622, Egypt

4. Department of Biochemistry, Biotechnology Research Institute, National Research Centre (NRC), 33 El Bohouth st., Dokki, Giza, 12622, Egypt

5. Department of Research on Children with Special Needs, Medical Research Institute, National Research Centre (NRC), 33 El Bohouth st., Dokki, Giza, 12622, Egypt

6. Department of Chemistry of Medicinal Plants, Pharmaceutical and Industries Research Institute, National Research Centre (NRC), 33 El Bohouth st., Dokki, Giza, 12622, Egypt

Abstract

Background Ashwagandha plant enhances the body’s defense against toxicants through improving the cell-mediated immunity. Objective The present work was performed to assess the protective and therapeutic efficiencies of ashwagandha seed extract (ASE) against the harmful effects of amoxicillin (AM) treatment on biological and physical parameters in the brain, liver, and testes tissues of rats. Materials and methods Total RNA was isolated from brain, liver, and testes tissues to assess the gene expression of steroid 5 alpha-reductase 1 (5α-R1), multidrug resistant 1b (mdr1b), and luteinizing hormone receptor (LHR) genes, respectively. The cDNA was synthesized and real-time polymerase chain reaction (Real-time PCR) was performed, total antioxidant capacity (TAC) was measured. Histological examination and physiological tests for the cerebral cortex of brain tissue were recorded. Results and conclusion Our findings revealed that AM treatment (90 mg/kg. b.wt.) caused detrimental effects in all biological parameters, including up-regulation of gene expressions and reduction of TAC values in brain, liver, and testes tissues, in addition to severe damage to histological architectures in the cerebral cortex, including hemorrhage and neurodegeneration. ASE treatment at different doses (100, 200, and 300 mg/kg) significantly enhanced the biological and physical parameters. As the ASE dose level increased, it was observed that these improvements in gene expressions and TAC also increased. Gene expression enhancements were more pronounced in the therapeutic efficacy of ASE, whereas TAC enhancements were more pronounced in the protective efficacy of this medicinal plant extract, particularly in brain and liver tissues. In terms of histopathological parameters, the damage caused by AM was reduced by using 300 mg/kg of protective ASE than 200 mg/kg of therapeutic ASE. Biophysical investigation indicated that relaxation time and enthalpy were restored and improved, while DC conductivity was not recovered by ASE use against AM damages. The present investigation provided biological and physical evidence for protective and therapeutic efficiencies of ASE against lesion effects of AM in the previously mentioned tissues of rats.

Publisher

Medknow

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