← 返回

Design, Synthesis, and Molecular Docking of Benzimidazole Derivatives as Angiotensin II AT1-Receptor Antagonists in a Hypertensive Rat Models.

Design, Synthesis, and Molecular Docking of Benzimidazole Derivatives as Angiotensin II AT1-Receptor Antagonists in a Hypertensive Rat Models.

期刊: Chemistry & biodiversity 日期: 2026-07-01 PMID: 42406979 DOI: 10.1002/cbdv.71455 浏览: 35
作者: Sarhan AE, Mohamed HS, Abdelhameed MF, Nagy AM, Abdelbaset M, Hamed MA
AE, S., HS, M., MF, A., AM, N., M, A., & MA, H. (2026). Design, Synthesis, and Molecular Docking of Benzimidazole Derivatives as Angiotensin II AT1-Receptor Antagonists in a Hypertensive Rat Models.. Chemistry & biodiversity. https://doi.org/10.1002/cbdv.71455
AE S, HS M, MF A, AM N, M A, MA H. Design, Synthesis, and Molecular Docking of Benzimidazole Derivatives as Angiotensin II AT1-Receptor Antagonists in a Hypertensive Rat Models.. Chemistry & biodiversity. 2026; doi: 10.1002/cbdv.71455
AE S, HS M, MF A, et al. Design, Synthesis, and Molecular Docking of Benzimidazole Derivatives as Angiotensin II AT1-Receptor Antagonists in a Hypertensive Rat Models.[J]. Chemistry & biodiversity. 2026. DOI: 10.1002/cbdv.71455.
@article{ae2026,
  author = {Sarhan AE and Mohamed HS and Abdelhameed MF and Nagy AM and Abdelbaset M and Hamed MA},
  title = {Design, Synthesis, and Molecular Docking of Benzimidazole Derivatives as Angiotensin II AT1-Receptor Antagonists in a Hypertensive Rat Models.},
  journal = {Chemistry & biodiversity},
  year = {2026},
  doi = {10.1002/cbdv.71455},
  note = {PMID: 42406979},
}
TY  - JOUR
AU  - Sarhan AE
AU  - Mohamed HS
AU  - Abdelhameed MF
AU  - Nagy AM
AU  - Abdelbaset M
AU  - Hamed MA
TI  - Design, Synthesis, and Molecular Docking of Benzimidazole Derivatives as Angiotensin II AT1-Receptor Antagonists in a Hypertensive Rat Models.
T2  - Chemistry & biodiversity
PY  - 2026
DO  - 10.1002/cbdv.71455
AN  - PMID:42406979
ER  - 

摘要

High blood pressure is a major risk factor of cardiovascular disorders. Experimental models of hypertension play a critical role in elucidating its pathophysiological mechanisms and in evaluating novel therapeutic agents. In this study, a series of benzimidazole-based derivatives (I- XIIIa-d) were designed and synthesized. The structural elucidation of the resulting pyrazoles, pyrimidines, diazepines, and isoxazoles were confirmed and examined against L-NAME induced hypertension in rats via targeting angiotensin II AT1 receptor comparing with Telmisartan as a reference drug. Significant reduction in systolic and diastolic blood pressure were observed upon treatment with VI, XIIIa, and XIIId compounds. Additionally, these compounds modulated the key signaling pathways involved in vascular remodeling, oxidative stress, and apoptosis by restoration of survival kinase signaling (Akt/GSK3β), enhancement of anti-apoptotic and anti-inflammatory regulators (BCL2, PPARγ), modulation of angiotensin receptor balance (AT1/ AT2), and attenuation of myocardial damage markers (CPK, LDH). The molecular docking showed that compounds VI, XIIIa, and XIIId had the strongest binding affinity against Ang II AT1 receptor. In conclusion, these findings suggest that the structural modifications of benzimidazole core can yield potent antihypertensive agents via a multi-mechanistic mode of action. They also emerge as promising candidates for further pharmacological development in hypertension treatment and cardiovascular complications.

AI 智能解读

相关文献

返回分类: 高血压 查看原文 (DOI)
已选择 0 篇文献