探究斑点型锌指结构蛋白（SPOP）介导Toll样受体（TLRs）/核因子κB（NF-κB）信号通路调控肺炎大鼠肺组织损伤的机制。

将30只Sprague Dawley大鼠分为肺炎组、抑制剂组和对照组，每组各10只。构建肺炎大鼠模型，观察大鼠肺组织病理学变化，并计算肺组织损伤程度评分及肺湿/干比重。采用western-blotting法检测SPOP、TLR4、TLR9、NF-κB及髓样分化因子88（MyD88）的蛋白表达，酶联免疫吸附法检测血清白细胞介素1β（IL-1β）、IL-6、肿瘤坏死因子α（TNF-α）水平。

对照组大鼠肺组织结构正常，无明显病变；肺炎组大鼠部分肺泡壁增厚，可观察到炎症细胞浸润；抑制剂组大鼠肺泡破坏程度更大，炎症细胞浸润范围和程度较肺炎组更重。3组大鼠肺组织损伤程度评分、湿/干比重，肺组织中SPOP、TLR4、TLR9、NF-κB、MyD88的蛋白表达水平以及血清IL-1β、IL-6、TNF-α水平比较，差异均有统计学意义（F = 178.049、8.557、15.489、36.935、37.490、35.152、91.250、89.687、361.539、16.319，P均< 0.001）。进一步两两比较发现，肺炎组及抑制剂组大鼠肺组织损伤程度评分、湿/干比重，肺组织中SPOP、TLR4、TLR9、NF-κB、MyD88的蛋白表达水平以及血清IL-1β、IL-6、TNF-α水平均高于对照组；且抑制剂组大鼠肺组织损伤程度评分、湿/干比重，肺组织中TLR4、TLR9、NF-κB、MyD88的蛋白表达水平以及血清IL-1β、IL-6、TNF-α水平均高于肺炎组，而SPOP的蛋白表达则低于肺炎组（P均< 0.05）。

SPOP通过与MyD88之间的相互作用调控TLRs/NF-κB信号通路，进而对肺炎大鼠肺组织的炎症反应造成影响。

To explore the mechanism of Toll-like receptors (TLRs)/nuclear factor-kappaB (NF-κB) signaling pathway mediated by speckle-type POZ protein (SPOP) on lung tissue injury in rats with pneumonia.

Thirty Sprague Dawley rats were divided into a pneumonia group, an inhibitor group and a control group, with 10 rats in each group. A rat model of pneumonia was constructed, and the histopathological changes of lung tissue were observed. The lung tissue injury degree score and lung wet/dry specific gravity were calculated. The protein expression levels of SPOP, TLR4, TLR9, NF-κB and myeloid differentiation factor 88 (MyD88) were detected by western-blotting. The levels of serum interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor-alpha (TNF-α) were detected by enzyme-linked immunosorbent assay.

The lung tissue structure of the rats in the control group was normal, without obvious lesions. In the pneumonia group, some alveolar walls were thickened, and inflammatory cell infiltration could be observed. The degree of alveolar destruction was greater, and the range and degree of inflammatory cell infiltration were more severe in the inhibitor group than in the pneumonia group. There were statistically significant differences in the lung tissue injury degree score, wet/dry specific gravity, protein expression levels of SPOP, TLR4, TLR9, NF-κB and MyD88 in lung tissue, and levels of serum IL-1β, IL-6 and TNF-α among the three groups (F = 178.049, 8.557, 15.489, 36.935, 37.490, 35.152, 91.250, 89.687, 361.539, 16.319; all P < 0.001). Further pairwise comparisons revealed that the lung tissue injury degree score, wet/dry specific gravity, and protein expression levels of SPOP, TLR4, TLR9, NF-κB, and MyD88 in lung tissue, as well as serum levels of IL-1β, IL-6 and TNF-α, in the pneumonia group and inhibitor group were all higher than those in the control group (all P < 0.05). Moreover, the lung tissue injury degree score, wet/dry specific gravity, and protein expression levels of TLR4, TLR9, NF-κB and MyD88 in lung tissue, as well as the levels of serum IL-1β, IL-6 and TNF-α, in the inhibitor group were all higher than those in the pneumonia group, while the protein expression of SPOP was lower (all P < 0.05).

SPOP regulates the TLRs/NF-κB signaling pathway through the interaction with MyD88, which in turn affects the inflammatory response of lung tissue in rats with pneumonia.