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东莨菪亭:一种经证实的通过调节PPAR-γ“多维方法”来抵御雨蛙肽诱导的急性胰腺炎及相关肺损伤的保护剂。

Scopoletin: A Validated Protector against Cerulein-induced Acute Pancreatitis & Associated Lung Injury by Regulating PPAR- γ "A Multidimensional Approach".

作者信息

Brahadeeswaran Subhashini, Chitluri Kiran Kumar, George Leema, Manickam Venkatraman, Emerson Isaac Arnold, Tamizhselvi Ramasamy

机构信息

School of Biosciences and Technology, Vellore Institute of Technology, Vellore, 632014, Tamil Nadu, India.

出版信息

Mol Biotechnol. 2024 Dec 2. doi: 10.1007/s12033-024-01327-y.

Abstract

Our previous study established the effectiveness of scopoletin (SC) in protecting mice against acute pancreatitis (AP) induced by cerulein and subsequent pulmonary injury. However, the precise molecular mechanisms underlying SC protective effects have yet to be elucidated. This research suggests that SC reduces the release of pro-inflammatory cytokines and nuclear factor kappa B (NF-κB) by activating the peroxisome proliferator-activated receptor γ (PPAR-γ) in mice suffering from AP. We observed the protective role of SC against the male Swiss mice with hourly intraperitoneal injections of cerulein (50 µg/kg) for six hours, followed by the administration of SC (10 mg/kg) one hour after AP induction, with or without the PPAR-γ antagonist GW9662 (0.3 mg/kg). The study exploration into the anti-inflammatory effects of SC revealed that a concentration of 25 µM enhanced the phagocytic clearance of dying pancreatic acinar cells by triggering the PPAR-γ signaling activation. Conversely, an in vitro assessment confirmed the presence of GW9662 counteracted the beneficial impact of SC on acinar cells. Molecular docking and simulation studies have shown that SC prompts significant structural changes in PPAR-γ. The in vivo, in vitro, and in silico analyses suggest that SC has potent anti-inflammatory properties that may be mediated by the activation of PPAR-γ signaling in cerulein-induced experimental pancreatitis.

摘要

我们之前的研究证实了东莨菪亭(SC)在保护小鼠免受雨蛙肽诱导的急性胰腺炎(AP)及后续肺损伤方面的有效性。然而,SC保护作用背后的确切分子机制尚未阐明。本研究表明,在患有AP的小鼠中,SC通过激活过氧化物酶体增殖物激活受体γ(PPAR-γ)来减少促炎细胞因子和核因子κB(NF-κB)的释放。我们观察了SC对雄性瑞士小鼠的保护作用,方法是每小时腹腔注射雨蛙肽(50µg/kg),持续6小时,然后在诱导AP1小时后给予SC(10mg/kg),同时或不给予PPAR-γ拮抗剂GW9662(0.3mg/kg)。对SC抗炎作用的研究发现,25µM的浓度通过触发PPAR-γ信号激活增强了对濒死胰腺腺泡细胞的吞噬清除。相反,体外评估证实GW9662的存在抵消了SC对腺泡细胞的有益影响。分子对接和模拟研究表明,SC促使PPAR-γ发生显著的结构变化。体内、体外和计算机模拟分析表明,SC具有强大的抗炎特性,可能是通过在雨蛙肽诱导的实验性胰腺炎中激活PPAR-γ信号介导的。

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