目的:探讨NLRP在光老化皮肤成纤维细胞表达变化和皮肤光老化机制中的作用。方法:2018年8月至2019年4月，在中山大学附属第三医院泌尿外科取3例儿童包皮环切术后包皮组织，分离培养成纤维细胞，并分为UVA照射组和空白对照组，UVA照射组接受连续UVA照射诱导慢性光损伤，空白对照组不接受UVA照射，通过CCK8试剂盒、β-半乳糖苷酶染色(SA-β-Gal)及细胞凋亡率检测验证建模。Western免疫印迹试验检测NLRP1、2、3、8蛋白表达。高通量测序技术检测调控NLRP炎症小体的非编码RNA表达变化。结果:UVA照射组细胞活性(70.0±4.7)%明显低于空白对照组(93.0±2.2)%，n t＝6.93，n P<0.05；细胞老化率(83.1±4.4)%高于空白对照组老化率(9.2±0.85)%(n t＝25.21，n P<0.05)；细胞凋亡率(34.5±7.1)%高于空白对照组 (9.3±2.2)%(n t＝6.42, n P<0.05)。蛋白定量检测结果显示，UVA照射组NLRP1、2、3、8表达较空白对照组(0.75±0.43)均上调，分别为5.59±0.99、3.84±0.69、9.98±1.72、1.57±0.56。高通量测序技术检测UVA照射组与空白对照组之间差异表达LncRNA，发现可调控NLRP炎症小体的长链非编码RNA中差异表达LncRNA共23个，其中变化最明显的为lnc-NLRP1、lnc-NLRP3。n 结论:反复UVA照射可上调NLRP炎症小体及其长链非编码LncRNA的表达，可通过参与活性氧自由基聚集、信号通路激活、自噬、基质金属蛋白酶/溶酶体组织蛋白酶家族表达及活性改变等机制，引起皮肤光老化。“,”Objective:To investigate the expression of NLRP inflammasome in skin photoaging mechanisms.Methods:Some cultured human dermal fibroblasts were subjected to repetitive ultraviolet A (UVA) radiation (UVA radiation group) to establish a photoaging cell model, which was then evaluated by cell counting kit 8 (CCK-8) assay, β-galactosidase staining and flow cytometry detection of apoptosis rate. Expression of NLRP1, NLRP2, NLRP3 and NLRP8 was detected via Western blot. High throughput sequencing was used to detect the expression of non-coding RNA (LncRNA) which regulates the inflammatory bodies of NLRP (Lnc-NLRP). The mean of two independent samples was compared by independent sample t test, and statistical significance was identified as n P<0.05.n Results:Compared with that in the control group, the UVA radiation group showed significantly decreased cellular proliferative activity (70±4.7)% vs. (93±2.2)%, n t=6.93, n P<0.05), but significantly increased apoptotic rate (34.5±7.1)% vs. (9.3±2.2)%,n t=6.42, n P<0.05). and percentage of β-galactosidase (83.1±4.4)%vs. (9.2±0.85)%,n t=25.21, n P<0.05). NLRP1, NLRP2, NLRP3 and NLRP8 expression was increased to 5.59±0.99, 3.84±0.69, 9.98±1.72, 1.57±0.56 compared to the control (0.75±0.43). Differentially expressed LncRNAs was detected via high throughput sequencing technique and found that 23 differentially expressed LncRNAs contributing to regulate NLRP inflammations among which the most obvious changes were lnc-NLRP1 and lnc-NLRP3.n Conclusions:Repeated UVA irradiation could up-regulate the expression of NLRP inflammasomes and LncNLRP which might take part in ROS aggregation, cell autophagy, MMPs/cathepsins expression and activity changes and signaling pathway activation process in skin photoaging mechanisms.