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Abstract：
UNASSIGNED: This study aims to determine whether Jianpi Qingre Tongluo Decoction (JQP) alleviates ankylosing spondylitis (AS) inflammation via the NONHSAT227927.1/JAK2/STAT3 axis.
UNASSIGNED: The effect of JQP on immune-inflammatory indicators in AS patients was explored through a combination of data mining, association rule analysis, and random walk model evaluation. Subsequently, network pharmacology and molecular docking were performed to screen out the potential signaling pathway. ELISA, PCR and wb were used to evaluate the effect of JQP on AS-FLS activity and inflammatory factors. The role of NONHSAT227927.1/JAK2/STAT3 combination in inflammation was studied by editing NONHSAT227927.1 and adding the JAK2/STAT3 inhibitor AG490. Involvement of the JAK2/STAT3 pathway was detected by PCR, WB, or immunofluorescence analysis.
UNASSIGNED: Retrospective data mining results show that JQP can effectively reduce the immune inflammatory response in AS patients. Through network pharmacology and molecular docking, it is speculated that JQP exerts its effect on AS through the JAK2/STAT3 pathway. Overexpression of NONHSAT227927.1 activated the JAK2/STAT3 pathway and promoted the expression of inflammatory factors, while serum containing JQP reversed the effects of NONHSAT227927.1 overexpression. NONHSAT227927.1 silencing inhibits the proliferation of AS-FLSs, inhibits the levels of inflammatory factors, and reduces the expression of JAK2/STAT3 protein. After adding the pathway blocker AG490, it was observed that the cell viability of AS-FLSs was reduced by inflammatory factors and the levels of JAK2/STAT3 were inhibited. , and overexpression of NONHSAT227927.1 can reverse this trend.
UNASSIGNED: JQP exerted an anti-inflammatory effect on AS by inhibiting the NONHSAT227927.1/JAK2/STAT3 axis.
UNASSIGNED: The effect of JQP on immune-inflammatory indicators in AS patients was explored through a combination of data mining, association rule analysis, and random walk model evaluation. Subsequently, network pharmacology and molecular docking were performed to screen out the potential signaling pathway. ELISA, PCR and wb were used to evaluate the effect of JQP on AS-FLS activity and inflammatory factors. The role of NONHSAT227927.1/JAK2/STAT3 combination in inflammation was studied by editing NONHSAT227927.1 and adding the JAK2/STAT3 inhibitor AG490. Involvement of the JAK2/STAT3 pathway was detected by PCR, WB, or immunofluorescence analysis.
UNASSIGNED: Retrospective data mining results show that JQP can effectively reduce the immune inflammatory response in AS patients. Through network pharmacology and molecular docking, it is speculated that JQP exerts its effect on AS through the JAK2/STAT3 pathway. Overexpression of NONHSAT227927.1 activated the JAK2/STAT3 pathway and promoted the expression of inflammatory factors, while serum containing JQP reversed the effects of NONHSAT227927.1 overexpression. NONHSAT227927.1 silencing inhibits the proliferation of AS-FLSs, inhibits the levels of inflammatory factors, and reduces the expression of JAK2/STAT3 protein. After adding the pathway blocker AG490, it was observed that the cell viability of AS-FLSs was reduced by inflammatory factors and the levels of JAK2/STAT3 were inhibited. , and overexpression of NONHSAT227927.1 can reverse this trend.
UNASSIGNED: JQP exerted an anti-inflammatory effect on AS by inhibiting the NONHSAT227927.1/JAK2/STAT3 axis.
摘要：
■本研究旨在确定健脾清热通络汤（JQP）是否通过NONHSAT227927.1/JAK2/STAT3轴缓解强直性脊柱炎（AS）炎症。
■通过结合数据挖掘，探讨了JQP对AS患者免疫炎症指标的影响，关联规则分析，和随机游走模型评价。随后，进行网络药理学和分子对接以筛选出潜在的信号通路。ELISA,PCR和wb评价JQP对AS-FLS活性和炎症因子的影响。通过编辑NONHSAT227927.1并添加JAK2/STAT3抑制剂AG490，研究了NONHSAT227927.1/JAK2/STAT3组合在炎症中的作用。通过PCR检测JAK2/STAT3通路的参与，WB,或免疫荧光分析。
■回顾性数据挖掘结果表明，JQP可以有效降低AS患者的免疫炎症反应。通过网络药理学和分子对接,推测JQP通过JAK2/STAT3通路对AS产生影响。过表达NONHSAT227927.1可激活JAK2/STAT3通路,促进炎症因子的表达,而含JQP的血清逆转了NONHSAT227927.1过表达的作用。NONHSAT227927.1沉默抑制AS-FLSs的增殖，抑制炎症因子的水平，并降低JAK2/STAT3蛋白的表达。添加途径阻断剂AG490后，观察到AS-FLSs的细胞活力被炎症因子降低，JAK2/STAT3水平受到抑制。,NONHSAT227927.1的过表达可以逆转这种趋势。
■JQP通过抑制NONHSAT227927.1/JAK2/STAT3轴对AS发挥抗炎作用。
■通过结合数据挖掘，探讨了JQP对AS患者免疫炎症指标的影响，关联规则分析，和随机游走模型评价。随后，进行网络药理学和分子对接以筛选出潜在的信号通路。ELISA,PCR和wb评价JQP对AS-FLS活性和炎症因子的影响。通过编辑NONHSAT227927.1并添加JAK2/STAT3抑制剂AG490，研究了NONHSAT227927.1/JAK2/STAT3组合在炎症中的作用。通过PCR检测JAK2/STAT3通路的参与，WB,或免疫荧光分析。
■回顾性数据挖掘结果表明，JQP可以有效降低AS患者的免疫炎症反应。通过网络药理学和分子对接,推测JQP通过JAK2/STAT3通路对AS产生影响。过表达NONHSAT227927.1可激活JAK2/STAT3通路,促进炎症因子的表达,而含JQP的血清逆转了NONHSAT227927.1过表达的作用。NONHSAT227927.1沉默抑制AS-FLSs的增殖，抑制炎症因子的水平，并降低JAK2/STAT3蛋白的表达。添加途径阻断剂AG490后，观察到AS-FLSs的细胞活力被炎症因子降低，JAK2/STAT3水平受到抑制。,NONHSAT227927.1的过表达可以逆转这种趋势。
■JQP通过抑制NONHSAT227927.1/JAK2/STAT3轴对AS发挥抗炎作用。
