Balkrishna Acharya, Sharma Sonam, Gohel Vivek, Singh Rani, Tomer Meenu, Dev Rishabh, Sinha Sandeep, Varshney Anurag
Drug Discovery and Development Division, Patanjali Research Foundation, Haridwar, India.
Department of Allied and Applied Sciences, University of Patanjali, Haridwar, India.
Animal Model Exp Med. 2025 Apr;8(4):728-738. doi: 10.1002/ame2.12472. Epub 2024 Jul 17.
Fever is characterized by an upregulation of the thermoregulatory set-point after the body encounters any pathological challenge. It is accompanied by uncomfortable sickness behaviors and may be harmful in patients with other comorbidities. We have explored the impact of an Ayurvedic medicine, Fevogrit, in an endotoxin (lipopolysaccharide)-induced fever model in Wistar rats.
Active phytoconstituents of Fevogrit were identified and quantified using ultra-high-performance liquid chromatography (UHPLC) platform. For the in-vivo study, fever was induced in male Wistar rats by the intraperitoneal administration of lipopolysaccharide (LPS), obtained from Escherichia coli. The animals were allocated to normal control, disease control, Paracetamol treated and Fevogrit treated groups. The rectal temperature of animals was recorded at different time points using a digital thermometer. At the 6-h time point, levels of TNF-α, IL-1β and IL-6 cytokines were analyzed in serum. Additionally, the mRNA expression of these cytokines was determined in hypothalamus, 24 h post-LPS administration.
UHPLC analysis of Fevogrit revealed the presence of picroside I, picroside II, vanillic acid, cinnamic acid, magnoflorine and cordifolioside A, as bioactive constituents with known anti-inflammatory properties. Fevogrit treatment efficiently reduces the LPS-induced rise in the rectal temperature of animals. The levels and gene expression of TNF-α, IL-1β and IL-6 in serum and hypothalamus, respectively, was also significantly reduced by Fevogrit treatment.
The findings of the study demonstrated that Fevogrit can suppress LPS-induced fever by inhibiting peripheral or central inflammatory signaling pathways and could well be a viable treatment for infection-induced increase in body temperatures.
发热的特征是身体在遇到任何病理挑战后体温调节设定点上调。它伴有令人不适的疾病行为,对患有其他合并症的患者可能有害。我们在Wistar大鼠的内毒素(脂多糖)诱导发热模型中探究了一种阿育吠陀药物Fevogrit的作用。
使用超高效液相色谱(UHPLC)平台对Fevogrit的活性植物成分进行鉴定和定量。在体内研究中,通过腹腔注射从大肠杆菌获得的脂多糖(LPS)诱导雄性Wistar大鼠发热。将动物分为正常对照组、疾病对照组、对乙酰氨基酚治疗组和Fevogrit治疗组。使用数字温度计在不同时间点记录动物的直肠温度。在6小时时间点,分析血清中TNF-α、IL-1β和IL-6细胞因子的水平。此外,在给予LPS后24小时,测定下丘脑这些细胞因子的mRNA表达。
Fevogrit的UHPLC分析显示,含有苦味素I、苦味素II、香草酸、肉桂酸、木兰碱和心叶岩白菜素A,这些作为具有已知抗炎特性的生物活性成分。Fevogrit治疗有效降低了LPS诱导的动物直肠温度升高。Fevogrit治疗还分别显著降低了血清和下丘脑中TNF-α、IL-1β和IL-6的水平及基因表达。
该研究结果表明,Fevogrit可通过抑制外周或中枢炎症信号通路来抑制LPS诱导的发热,很可能是治疗感染引起体温升高的一种可行疗法。