Mehta Jinay Paresh, Kagal Urmila Anil, Biradar Prakash R
Department of Pharmacology, KLE Academy of Higher Education and Research, Deemed-to-be-University, Jawaharlal Nehru Medical College, Belagavi, Karnataka, India.
Department of Pharmacology, KLE Academy of Higher Education and Research, Deemed-to-be-University, KLE College of Pharmacy, Belagavi, Karnataka, India.
Int J Appl Basic Med Res. 2025 Jan-Mar;15(1):25-31. doi: 10.4103/ijabmr.ijabmr_330_24. Epub 2025 Jan 9.
Depression affects millions globally, with existing treatments having many side effects. (WS) shows potential as an antidepressant and neuroprotective agent, possibly by influencing brain-derived neurotrophic factor (BDNF)-related pathways.
This study evaluated the effect of WS alone and in combination with fluoxetine on neuritin, NARP, and BDNF Exon-III gene expression in the hippocampus of male Wistar rats subjected to chronic unpredictable mild stress (CUMS).
Thirty male Wistar rats were divided into five groups ( = 6 each): normal group (NG), disease control (DC), standard treatment (ST), WS, and combination group of fluoxetine and WS (FW). Depression was induced using CUMS, except in the NG. The sucrose preference test confirmed depression at the end of 3 week and assessed treatment effects at the end of 7 week. Gene expression in the hippocampus was analyzed through real-time PCR at the end of 7 week.
After 7 weeks, the ST, WS, and FW groups showed a significant increase in sucrose preference compared to the DC group. The ST and FW groups showed significant upregulation of all three genes selected in the present study. Comparison between NG and FW groups showed no significant difference in gene expression.
This study highlights the antidepressant effects of WS by demonstrating its effect on BDNF-associated gene expression. Fluoxetine combined with WS demonstrated additive effects which proves an adjuvant role of WS in the treatment of depression. Further studies involving human subjects are essential to validate the antidepressant effects of WS and its additive effects with fluoxetine.
抑郁症影响着全球数百万人，现有治疗方法有许多副作用。（WS）显示出作为一种抗抑郁和神经保护剂的潜力，可能是通过影响脑源性神经营养因子（BDNF）相关途径。
本研究评估了WS单独以及与氟西汀联合使用对遭受慢性不可预测轻度应激（CUMS）的雄性Wistar大鼠海马中神经突蛋白、NARP和BDNF外显子III基因表达的影响。
30只雄性Wistar大鼠分为五组（每组n = 6）：正常组（NG）、疾病对照组（DC）、标准治疗组（ST）、WS组以及氟西汀与WS联合组（FW）。除NG组外，使用CUMS诱导抑郁症。在3周结束时通过蔗糖偏好试验确认抑郁症，并在7周结束时评估治疗效果。在7周结束时通过实时PCR分析海马中的基因表达。
7周后，与DC组相比，ST组、WS组和FW组的蔗糖偏好显著增加。ST组和FW组在本研究中选择的所有三个基因均显著上调。NG组和FW组之间的基因表达无显著差异。
本研究通过证明WS对BDNF相关基因表达的影响，突出了其抗抑郁作用。氟西汀与WS联合显示出相加效应，这证明了WS在抑郁症治疗中的辅助作用。涉及人类受试者的进一步研究对于验证WS的抗抑郁作用及其与氟西汀的相加效应至关重要。
