MedElevator
Войти в исследования Journal of inflammation research · 2026
Shengjiangsan Upregulates miR-328-3p to Inhibit MAP3K9 in the Treatment of Sjogren Disease: A Bioinformatics Analysis.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Ren Yating, Wang Yihan, Hong Tao, Jiao Wenyue, Lu Dingqi, Yao Xinyi, Zhou Donghai, Wang Xinchang
Аннотация
OBJECTIVE: Conventional treatments for Sjögren's disease (SjD) have limited therapeutic efficacy, whereas Shengjiangsan (SJS) has been reported to ameliorate SjD, although further research is lacking. The aim of the present study was to investigate the effects exerted by, and underlying mechanisms of, SJS in the treatment of SjD through miRNA sequencing, bioinformatics analysis, and in vitro and in vivo experiments.
METHODS: Key miRNAs and their target genes involved in the effects of SJS on SjD were identified through microRNA sequencing and bioinformatics analysis, and their targeting relationships were verified using a dual-luciferase assay. Animal and cell experiments were conducted to demonstrate the efficacy and underlying mechanisms of SJS in treating SjD.
RESULTS: RNA sequencing showed that the expression of miR-328-3p in the model group with SjD was low and upregulated after SJS treatment, reaching levels comparable to those in the control group. Expression of its target gene, MAP3K9, was elevated in the model group and decreased after treatment. Simultaneously, dual-luciferase assays verified the targeting relationship between miR-328-3p and MAP3K9, and cell transfection experiments demonstrated that SJS inhibited MAP3K9 expression by increasing miR-328-3p levels. Additionally, experiments showed that SJS significantly increased the salivary flow rate in SjD mice, reduced inflammatory infiltration of SG lymphocytes, enhanced AQP5 protein expression, and decreased serum levels of inflammatory factors such as IgG, BAFF, IL-6, and IFN-γ.
CONCLUSION: SJS may targets miR-328-3p to inhibit MAP3K9 expression, alleviate inflammation in NOD/Ltj mice, reduce pathological damage in the SG, increase saliva secretion, and improve SjD symptoms.
METHODS: Key miRNAs and their target genes involved in the effects of SJS on SjD were identified through microRNA sequencing and bioinformatics analysis, and their targeting relationships were verified using a dual-luciferase assay. Animal and cell experiments were conducted to demonstrate the efficacy and underlying mechanisms of SJS in treating SjD.
RESULTS: RNA sequencing showed that the expression of miR-328-3p in the model group with SjD was low and upregulated after SJS treatment, reaching levels comparable to those in the control group. Expression of its target gene, MAP3K9, was elevated in the model group and decreased after treatment. Simultaneously, dual-luciferase assays verified the targeting relationship between miR-328-3p and MAP3K9, and cell transfection experiments demonstrated that SJS inhibited MAP3K9 expression by increasing miR-328-3p levels. Additionally, experiments showed that SJS significantly increased the salivary flow rate in SjD mice, reduced inflammatory infiltration of SG lymphocytes, enhanced AQP5 protein expression, and decreased serum levels of inflammatory factors such as IgG, BAFF, IL-6, and IFN-γ.
CONCLUSION: SJS may targets miR-328-3p to inhibit MAP3K9 expression, alleviate inflammation in NOD/Ltj mice, reduce pathological damage in the SG, increase saliva secretion, and improve SjD symptoms.