Chowdhury Sejuti Ray, Ghosh Sourav, Chatterjee Shilpa, Murtuja Sheikh, Rakshit Gourav, Basu Biswajit, Prajapati Bhupendra, Ali Nemat
Department of Pharmaceutical Technology, School of Health & Medical Sciences, Adamas University, Kolkata, West Bengal, India.
Department of Pharmaceutical Science and Technology, Birla Institute of Technology, Mesra, Ranchi, Jharkhand, India.
Chem Biodivers. 2025 Aug;22(8):e202402842. doi: 10.1002/cbdv.202402842. Epub 2025 Apr 14.
This study discovers the potential of hydroxychavicol-enriched fraction of Piper betle L. leaf extract (HCRF) as an antidepressant alternative in chronic unpredictable mild stress (CUMS) rodent models with biochemical parameters. It also focused on possible mechanisms through molecular simulation via the anti-inflammatory pathway and in silico pharmacokinetic study. HCRF is isolated from betel leaves, and Swiss albino mice were orally administrated with doses of 50 mg/kg and 100 mg/kg of body weight (bw) for 5 weeks before the CUMS protocols, respectively. In silico investigation is done with pkCSM software for the ADMET study, and molecular docking is performed on hydroxychavicol with target protein 2ZOQ in Schrödinger. HCRF prevented the irregular behaviors acquired in CUMS model, with reduced hypoactivity and sucrose anhedonia. HCRFs of 50 and 100 mg/kg bw diminished the upsurges in the level of tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) in the serum associated with stress. HCRF of 100 mg/kg bw improved inflammation in the brain by plummeting the malonaldehyde and increasing the glutathione via revering oxidative stress. HCRF exhibited an activity similar to antidepressants and might be a consequence of the anti-inflammatory action. The molecular simulation and pharmacokinetic study ensured a probable mechanistic approach of hydroxychavicol in CUMS-associated depression through inflammatory pathways.
本研究发现,在具有生化参数的慢性不可预测轻度应激(CUMS)啮齿动物模型中,蒌叶提取物富含羟基查维酮的部分(HCRF)具有作为抗抑郁替代物的潜力。研究还通过抗炎途径的分子模拟和计算机模拟药代动力学研究,聚焦于其可能的作用机制。HCRF从蒌叶中分离得到,在进行CUMS实验方案前,分别以50毫克/千克和100毫克/千克体重(bw)的剂量对瑞士白化小鼠进行5周的口服给药。使用pkCSM软件进行计算机模拟ADMET研究,并在薛定谔软件中对羟基查维酮与靶蛋白2ZOQ进行分子对接。HCRF预防了CUMS模型中出现的异常行为,减少了活动减退和蔗糖快感缺失。50毫克/千克bw和100毫克/千克bw的HCRF降低了与应激相关的血清中肿瘤坏死因子α(TNF-α)和白细胞介素-1β(IL-1β)水平的升高。100毫克/千克bw的HCRF通过降低丙二醛水平和通过逆转氧化应激增加谷胱甘肽来改善大脑炎症。HCRF表现出与抗抑郁药相似的活性,这可能是其抗炎作用的结果。分子模拟和药代动力学研究确保了羟基查维酮在CUMS相关抑郁症中通过炎症途径的可能作用机制。