The present study utilizes network pharmacology and molecular docking methodologies to investigate the mechanism of action behind the intervention of Polygonum capitatum Buch.-Ham.ex D. Don (THL) in treating pulmonary nodules (PN). This research aims to provide a theoretical foundation for broadening the clinical application of THL. Active components of THL were identified and screened through an extensive literature review and the PharmMapper database, followed by an analysis of their target interactions. Relevant targets associated with PN were selected using databases such as OMIM and GeneCards, with an intersection of the two sets being determined. STRING11.5 facilitated the acquisition of protein-protein interaction data, which was then imported into Cytoscape 3.7.2 to establish a protein interaction network topology. This enabled the identification of pivotal targets affected by THL intervention in PN. The study further employed the Metascape database to conduct GO and KEGG bioinformatics enrichment analyses, which illuminated core pathways involved in THL's therapeutic effects on PN. A comprehensive component-target-pathway diagram was constructed utilizing Cytoscape 3.7.2 software, with molecular docking validations carried out via Maestro software. A total of 49 active THL ingredients were discerned, implicating 67 PN-relevant targets. Subsequent software analysis pinpointed 10 key targets, including ALB, EGFR, and SRC. Molecular docking studies indicated strong binding affinities for most protein-compound pairs, with 44 out of 60 docking results exhibiting binding energies below -5 kcal/mol. Enrichment analysis highlights that key targets are mainly involved in pathways such as cancer, lipid metabolism and atherosclerosis, estrogen signaling, IL-17 signaling, complement and coagulation cascades, and chemical carcinogenesis through receptor activation. Through comprehensive network pharmacological approaches, this research delineates the synergy of THL's multiple components, targets, and pathways in mitigating PN. It posits that primary active ingredients of THL - quercetin, salidroside, and oleanolic acid - may exert effects on targets like ALB, EGFR, SRC, potentially modulating pathways associated with cancer, lipid and atherosclerosis, and IL-17 signaling in the context of PN intervention.

头花蓼为贵州传统苗药,具有清热利湿、利水通淋等功效.其主要化学成分为黄酮类、木脂素类及挥发油类,还含有萜类、鞣质类等成分.近年来,因头花蓼具有抗炎、抗菌、抗氧化及降血糖等多种药理作用而成为研究热点.研究头花蓼相关国内外文献,综述其化学成分及药理作用机制,以期对头花蓼的药理研究及临床应用提供参考.

目的 研究骨碎补对庆大霉素耳毒性豚鼠耳蜗VDR、CYP27B1及CYP24A1的影响.方法 将30只成年健康雄性豚鼠随机均分为空白组,模型组,骨碎补低、中、高剂量组,维生素D组.空白组腹腔注射生理盐水,其他各组腹腔注射庆大霉素进行造模,均持续21 d.空白组与模型组予生理盐水灌胃;骨碎补低、中、高剂量组,依次予不同剂量的骨碎补灌胃;维生素D组予维生素D灌胃,均持续21 d.采用HE染色法观察豚鼠耳蜗组织病理改变;采用免疫组化法检测耳蜗组织VDR、CYP27B1、CYP24A1蛋白表达情况.结果 与空白组比较,模型组豚鼠有明显耳组织病理改变,耳蜗组织VDR、CYP27B1蛋白表达均降低,CYP24A1蛋白表达升高(P＜0.01).与模型组比较,骨碎补中剂量组及维生素D组耳蜗组织病理改变不同程度减轻,耳蜗组织VDR、CYP27B1蛋白表达水平升高,CYP24A1蛋白表达水平降低(P＜0.01).结论 骨碎补可改善庆大霉素耳毒性影响的豚鼠耳蜗组织,其机制可能与维生素D相关蛋白表达有关.

目的 探讨热淋清颗粒对脓毒症急性肺损伤模型大鼠的保护作用及其机制.方法 将30只SD大鼠随机分为6组:假手术组、模型组、热淋清颗粒高剂量组[4.8 g/(kg·d)]、热淋清颗粒中剂量组[2.4 g/(kg·d)]、热淋清颗粒低剂量组[1.2 g/(kg·d)]、阳性对照组[地塞米松1.5 mg/(kg·d)],每组5只.各组均采用灌胃给药,1次/d,连续给药7 d,末次给药后各组大鼠均采用盲肠结扎穿孔法制备脓毒症急性肺损伤模型(假手术组不结扎和穿孔),造模24 h后取材.取各组大鼠右肺中叶计算肺组织湿/干重比;采用HE染色法观察各组大鼠肺组织病理学改变并进行损伤评分;采用ELISA法检测各组大鼠血清中IL-1α、TNF-α、PGE2水平含量;采用RT-PCR法检测各组大鼠肺组织中TLR4、MyD88、NF-κB p65 mRNA相对表达量;采用Western-Blot检测各组大鼠肺组织中TLR4、MyD88、NF-κB p65蛋白相对表达量.结果 与假手术组比较,模型组大鼠肺组织湿/干重比、肺组织病理损伤评分显著升高(P＜0.01);与模型组比较,热淋清颗粒高剂量组和阳性对照组可显著降低大鼠肺组织湿/干重比、肺组织病理损伤评分(P＜0.05);与假手术组比较,模型组大鼠血清TNF-α、IL-1α、PGE2水平及肺组织TLR4、MyD88、NF-KB p65 mRNA和蛋白表达量均显著升高(P＜0.01);与模型组比较,热淋清颗粒高、中剂量组和阳性对照组大鼠血清TNF-α、IL-1α、PGE2水平及肺组织TLR4、MyD88、NF-κB p65 mRNA和蛋白表达量显著降低(P＜0.05);热淋清颗粒高剂量组上述各指标改善情况优于阳性对照组.结论 热淋清颗粒能减轻脓毒症大鼠急性肺损伤,其机制可能与调节TLR4/MyD88/NF-κB p65通路有关.

Pulmonary fibrosis (PF) is a serious interstitial disease that includes diffuse collagen deposition of lung tissue. Polygonum capitatum Buch.-Ham. ex D. Don (THL) is a traditional vaccine that has antibacterial and anti-inflammatory effects. In this research, to investigate the mechanism of action of THL in the intervention of pulmonary fibrosis by network pharmacology and molecular docking related research methods, in order to provide a theoretical basis for expanding the scope of THL medication. A total of 49 active ingredients were analyzed and screened in Cephalus cephalusis , including 35 pulmonary fibrosis targets, and 10 key targets such as ALB, EGFR were screened after software analysis. The molecular docking results showed that there were 44 binding energies less than –3 kcal·mol −1 in the 60 docking results, indicating that most proteins had strong binding energies with compounds. The key targets of KEGG enrichment analysis were mainly enriched in 20 core action pathways, such as hemostasis-related pathway, regulation of kinase activity. This study shows that based on network pharmacology, the multicomponent–multitarget–multipathway effect of THL intervention in pulmonary fibrosis is discussed.

目的 探讨热淋清颗粒对干酵母致热模型大鼠的解热作用及其作用机制.方法 采用颈背部皮下注射干酵母悬浊液法复制大鼠发热模型,将60只SD大鼠随机分为正常组、模型组、阳性对照组和热淋清颗粒高、中、低剂量组,每组10只,雌雄各半.检测造模后不同时间点大鼠体温,ELISA法检测血清中肿瘤坏死因子-α(TNF-α)、精氨酸加压素(AVP)及下丘脑中的前列腺素E2(PGE2)、环磷酸腺苷(cAMP)水平.结果 模型组大鼠体温、血清中TNF-α、AVP含量、下丘脑中PGE2、cAMP含量均较正常组显著上升(P<0.01);热淋清颗粒高、中剂量组大鼠体温、血清中TNF-α及下丘脑中PGE2、cAMP含量均较模型组显著降低(P<0.01);热淋清颗粒抑制发热大鼠体温上升在一定范围内存在量效关系;与模型组比较,热淋清颗粒高剂量组AVP水平显著升高(P<0.01).结论 热淋清颗粒具有良好的解热作用且高剂量效果最优,其作用机制可能是通过抑制机体内生热源TNF-α生成,降低体温中枢正调节介质PGE2、cAMP分泌水平,促进机体体温调节介质AVP的分泌而达到解热作用.