Department of Pharmacology, College of Pharmacy, University of Sargodha, Sargodha, Pakistan.
Institute of Pharmacy, Lahore College for Women University, Lahore, Pakistan.
Inflammopharmacology. 2024 Dec;32(6):3761-3784. doi: 10.1007/s10787-024-01569-x. Epub 2024 Sep 29.
The current study aimed to evaluate the anti-inflammatory, anti-oxidant, and pronounced gastro-protective activities of β- Citronellol using in vitro, in vivo assays and in silico approaches.
In vitro assays, denaturation of bovine serum albumin, egg protein, and human Red Blood Cells (RBCs) membrane stabilization were performed, using Piroxicam as standard. For in vivo assessment, Histamine (0.1 ml from 1% w/v) and Formaldehyde (0.1 ml from 2% v/v) were used to mediate inflammation. In silico molecular docking and network pharmacology were employed to probe the possible target genes mediating gastroprotective effect of β-Citronellol at 25, 50, and 100 mg/kg, using indomethacin-induced (25 mg/kg i.p) gastric ulcer in rats. Moreover, Gastric tissues were evaluated for morphological, histopathological, and bio-chemical analysis of PGE COX-I, COX-II, 5-LOX, eNOS, ICAM-1, oxygen-free radical scavengers (SOD, CAT), and oxidative stress marker (MDA).
β-Citronellol prevented denaturation of proteins and RBCs membrane stabilization with maximum effect observed at 6,400 µg/mL. Citronellol decreased rat's paw edema. Network pharmacology and docking studies revealed gastro-protective potential of Citronellol possibly mediated through arachidonic acid pathways by targeting COX-I, COX-II, PGE, and 5-LOX. Citronellol reduced the ulcer indices, and histopathological changes. Further, β-Citronellol (50 and 100 mg/kg) increased gastric PGE COX-1, and eNOS; while suppressing COX-2, 5-LOX and ICAM-1. Citronellol markedly enhanced the oxidative balance in isolated rat stomach tissues.
The anti-inflammatory, anti-oxidant, and gastro-protective effects of β-Citronellol against indomethacin-induced gastric ulcer model in rats through mediating COX-I, COX-II, PGE 5-LOX, eNOS, and ICAM-1 inflammatory markers.
本研究旨在通过体外、体内试验和计算方法评估β-香茅醇的抗炎、抗氧化和显著的胃保护活性。
使用吡罗昔康作为标准，进行体外试验，包括牛血清白蛋白、卵蛋白和人红细胞（RBC）膜的变性、稳定性测定。对于体内评估，使用组胺（0.1ml 来自 1%w/v）和甲醛（0.1ml 来自 2%v/v）介导炎症。使用吲哚美辛（25mg/kg i.p）诱导的大鼠胃溃疡模型，在 25、50 和 100mg/kg 下，通过计算分子对接和网络药理学研究β-香茅醇对胃保护作用的可能靶基因。此外，还评估了胃组织的形态学、组织病理学和生物化学分析，包括 PGE COX-I、COX-II、5-LOX、eNOS、ICAM-1、氧自由基清除剂（SOD、CAT）和氧化应激标志物（MDA）。
β-香茅醇防止了蛋白质变性和 RBC 膜的稳定性，最大效应观察到在 6400μg/ml。香茅醇降低了大鼠的爪肿胀。网络药理学和对接研究表明，香茅醇可能通过靶向 COX-I、COX-II、PGE 和 5-LOX，通过花生四烯酸途径发挥胃保护作用。香茅醇降低了溃疡指数和组织病理学变化。此外，β-香茅醇（50 和 100mg/kg）增加了胃 PGE COX-1 和 eNOS；同时抑制 COX-2、5-LOX 和 ICAM-1。香茅醇显著增强了分离大鼠胃组织中的氧化平衡。
β-香茅醇通过调节 COX-I、COX-II、PGE 5-LOX、eNOS 和 ICAM-1 炎症标志物，对吲哚美辛诱导的大鼠胃溃疡模型具有抗炎、抗氧化和胃保护作用。
