{"title":"Laggera alata Attenuates Inflammatory Response by Regulating Macrophage Polarization in Rheumatoid Arthritis Mice.","authors":"Jiangcun Wei, Yunli Tang, Suhong Qin, Xiumei Ma, Wen Zhong, Peng Yang, Qingmei Deng, Jiabao Ma","doi":"10.1007/s12033-023-00808-w","DOIUrl":null,"url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a type of joint injury, which can induce the activation of inflammatory factors and polarization of tissue macrophages. Total phenolics from Laggera alata (TPLA) has been reported to exhibit anti-inflammatory effect in various diseases. However, its specific function in RA is still unknown. Here, the protective properties of TPLA were studied in collagen-induced arthritis (CIA)-induced RA mice. RA mouse model was established through the CIA induction. Arthritis score, hind paw thickness, and the body weight of the RA mice were evaluated in each group. H&E staining was conducted in hind paw and joint tissues for histopathological staining. The distal femur was analyzed by microCT, and bone loss-related indicators were assessed. The expression of macrophage polarization markers was detected by immunofluorescence staining in RA mice. The serum levels of inflammatory markers were determined by enzyme-linked immunosorbent assay (ELISA). TPLA reduced the CIA-induced arthritis score and hind paw thickness in mice. The body weight of the CIA mouse was significantly increased by TPLA treatment. TPLA improved the CIA-induced histopathological changes in the hind paw and joint tissues from the mice. TPLA inhibited the bone loss and alleviated bone destruction in CIA mouse model. TPLA altered the macrophage phenotype from M1 macrophages into M2 in CIA mice. TPLA suppressed the levels of inflammatory markers both in the serum and joint tissues of the CIA mice. TPLA mitigated RA development by suppressing inflammatory reaction through the inhibition of M1 microphage polarization.</p>","PeriodicalId":18865,"journal":{"name":"Molecular Biotechnology","volume":null,"pages":null},"PeriodicalIF":2.4000,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular Biotechnology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12033-023-00808-w","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/7/26 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Rheumatoid arthritis (RA) is a type of joint injury, which can induce the activation of inflammatory factors and polarization of tissue macrophages. Total phenolics from Laggera alata (TPLA) has been reported to exhibit anti-inflammatory effect in various diseases. However, its specific function in RA is still unknown. Here, the protective properties of TPLA were studied in collagen-induced arthritis (CIA)-induced RA mice. RA mouse model was established through the CIA induction. Arthritis score, hind paw thickness, and the body weight of the RA mice were evaluated in each group. H&E staining was conducted in hind paw and joint tissues for histopathological staining. The distal femur was analyzed by microCT, and bone loss-related indicators were assessed. The expression of macrophage polarization markers was detected by immunofluorescence staining in RA mice. The serum levels of inflammatory markers were determined by enzyme-linked immunosorbent assay (ELISA). TPLA reduced the CIA-induced arthritis score and hind paw thickness in mice. The body weight of the CIA mouse was significantly increased by TPLA treatment. TPLA improved the CIA-induced histopathological changes in the hind paw and joint tissues from the mice. TPLA inhibited the bone loss and alleviated bone destruction in CIA mouse model. TPLA altered the macrophage phenotype from M1 macrophages into M2 in CIA mice. TPLA suppressed the levels of inflammatory markers both in the serum and joint tissues of the CIA mice. TPLA mitigated RA development by suppressing inflammatory reaction through the inhibition of M1 microphage polarization.
类风湿性关节炎（RA）是一种关节损伤，可诱导炎症因子的激活和组织巨噬细胞的极化。有报道称，从扁柏中提取的总酚类化合物（TPLA）在多种疾病中具有抗炎作用。然而，它在 RA 中的具体功能尚不清楚。在此，研究了 TPLA 在胶原诱导关节炎（CIA）诱导的 RA 小鼠中的保护特性。通过 CIA 诱导建立了 RA 小鼠模型。对各组 RA 小鼠的关节炎评分、后爪厚度和体重进行评估。对小鼠后爪和关节组织进行 H&E 染色，以进行组织病理学染色。用显微CT分析股骨远端，评估骨质流失相关指标。通过免疫荧光染色检测 RA 小鼠巨噬细胞极化标记物的表达。通过酶联免疫吸附试验（ELISA）测定血清中炎症标志物的水平。TPLA 降低了 CIA 诱导的小鼠关节炎评分和后爪厚度。TPLA治疗后，CIA小鼠的体重明显增加。TPLA 改善了 CIA 诱导的小鼠后爪和关节组织病理变化。TPLA 可抑制 CIA 小鼠模型的骨质流失并减轻骨质破坏。TPLA 可改变 CIA 小鼠的巨噬细胞表型，使其从 M1 型巨噬细胞转变为 M2 型巨噬细胞。TPLA 可抑制 CIA 小鼠血清和关节组织中的炎症标志物水平。TPLA 通过抑制 M1 型巨噬细胞的极化来抑制炎症反应，从而缓解 RA 的发展。
期刊介绍：
Molecular Biotechnology publishes original research papers on the application of molecular biology to both basic and applied research in the field of biotechnology. Particular areas of interest include the following: stability and expression of cloned gene products, cell transformation, gene cloning systems and the production of recombinant proteins, protein purification and analysis, transgenic species, developmental biology, mutation analysis, the applications of DNA fingerprinting, RNA interference, and PCR technology, microarray technology, proteomics, mass spectrometry, bioinformatics, plant molecular biology, microbial genetics, gene probes and the diagnosis of disease, pharmaceutical and health care products, therapeutic agents, vaccines, gene targeting, gene therapy, stem cell technology and tissue engineering, antisense technology, protein engineering and enzyme technology, monoclonal antibodies, glycobiology and glycomics, and agricultural biotechnology.
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