| 司晴,王桂华,张铁征,等.宁心缓痛汤对子宫内膜异位症痛经疼痛、细胞焦亡及 NLRP3炎性小体的影响[J].安徽医药,2025,29(3):482-487. |
| 宁心缓痛汤对子宫内膜异位症痛经疼痛、细胞焦亡及 NLRP3炎性小体的影响 |
| Effect of Ningxin Huantong Tang on dysmenorrhea pain, cell pyroptosis, and NLRP3 inflammasome in endometriosis |
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| DOI：10.3969/j.issn.1009-6469.2025.03.011 |
| 中文关键词: 子宫内膜异位症 宁心缓痛汤 核苷酸结合结构域富含亮氨酸重复序列和含热蛋白结构域受体 3 细胞焦亡 痛经 疼痛反应 前列腺素 |
| 英文关键词: Endometriosis Ningxin Huantong Tang NLRP3 Cell pyroptosis Dysmenorrhea Pain response Prostaglandins |
| 基金项目:衡水市科技计划项目( 14027A) |
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| 中文摘要: |
| 目的探究宁心缓痛汤调控核苷酸结合结构域富含亮氨酸重复序列和含热蛋白结构域受体 3(NLRP3)炎性小体介导的细胞焦亡对子宫内膜异位症痛经大鼠疼痛反应的影响。方法 2022年 1月至 2023年 5月，采用随机数字表法将 50只大鼠分为假手术组 10只和造模组 40只。造模组在造模过程中有 3只大鼠造模失败、 1只大鼠死亡，造模成功后的 36只大鼠采用随机数字表法分成四组:子宫内膜异位症疼痛大鼠模型组( EMT组)、低剂量宁心缓痛汤干预组(宁心缓痛汤 -L组)、高剂量宁心缓痛汤干预组(宁心缓痛汤 -H组)和孕三烯酮组，每组各 9只。检测各组大鼠痛经状况和血清中前列腺素 F2α(PGF2α)和前列腺素 E2(PGE2)含量；苏木精 -伊红(HE)染色检测异位子宫内膜组织病理学变化；末端脱氧核苷酸转移酶(TUNEL)检测异位子宫内膜组织细胞凋亡；蛋白质印迹法检测异位子宫内膜组织中胱天蛋白酶 -1(caspase-1)、 NLRP3、Gasdermin D(GSDMD)、白细胞介素( IL)-1β、IL-18蛋白表达。结果和假手术组相比， EMT组大鼠扭体次数、血清中 PGF2α含量［( 208.91±17.06)ng/L比(115.36±10.27)ng/L］和 PGF2α/PGE2(0.97±0.10比 0.27±0.03)、异位子宫内膜组织中细胞凋亡率和 NLRP3(0.81±0.09比 0.15±0.02)、 caspase-1(0.73±0.08比 0.12±0.02)、 GSDMD(0.91±0.11比 0.30±0.03)、 IL(白细胞介素) -1β(1.21±0.12比 0.24±0.03)、 IL-18蛋白( 0.92±0.10比 0.26±0.03)表达明显增加，疼痛潜伏期、血清中 PGE2含量［( 214.31±19.52)ng/L比( 423.78±35.61)ng/L］明显减少( P<0.05)；和 EMT组相比，宁心缓痛汤 -L组、宁心缓痛汤 -H组和孕三烯酮组大鼠扭体次数、血清中 PGF2α含量和 PGF2α/ PGE2、异位子宫内膜组织中细胞凋亡率和 NLRP3、caspase-1、GSDMD、IL-1β、IL-18蛋白表达明显减少，疼痛潜伏期、血清中 PGE2含量明增加( P<0.05)。结论宁心缓痛汤可能通过抑制 NLRP3介导的细胞焦亡，减轻炎症反应，调控血清中的 PGE2、 PGF2α的合成与释放，从而对子宫内膜异位症痛经大鼠发挥一定的治疗作用。 |
| 英文摘要: |
| Objective To investigate the effect of Ningxin Huantong Tang on the pain response of endometriosis dysmenorrhea ratsby regulating the inflammatory cell death mediated by nucleotide binding oligomerization domain receptor 3 (NLRP3) inflammasome.Methods From January 2022 to May 2023, Using a random number table method, 50 rats were divided into a sham surgery group of10 rats and a modeling group of 40 rats. During the modeling process, 3 rats failed and 1 rat died. After successful modeling, the 36 ratswere randomly divided into four groups using a random number table: endometriosis pain rat model group (EMT group), low-dose Ningx. in Huantong Tang intervention group (Ningxin Huantong Tang-L group), high-dose Ningxin Huantong Tang intervention group (Ningx. in Huantong Tang-H group), and gestrinone group, with 9 rats in each group. The dysmenorrhea status and serum levels of prostaglan-din F2 alpha (PGF2 alpha) and prostaglandin E2 (PGE2) in each group of rats were detected; Hematoxylin eosin (HE) staining was usedto detect pathological changes in ectopic endometrial tissue; Terminal deoxynucleotide transferase (TUNEL) was used to detect apopto-sis in ectopic endometrial tissue cells; Western blotting was used to detect the protein expression of cysteine containing aspartic acidprotease (caspase-1), NLRP3, Gasdermin D (GSDMD), interleukin-1β (IL-1β), and interleukin-18 (IL-18) in ectopic endometrial tissue. Results Compared with the sham surgery group, the number of body twists, serum PGF2 α content [(208.91±17.06) ng/L vs. (115.36± 10.27) ng/L], PGF2α/PGE2 ratio (0.97±0.10 vs. 0.27±0.03), apoptosis rate and NLRP3 (0.81±0.09 vs. 0.15±0.02), caspase-1 (0.73±0.08 vs. 0.12±0.02), GSDMD (0.91±0.11 vs. 0.30±0.03), IL-1β (1.21±0.12 vs. 0.24±0.03), IL-18 protein (0.92±0.10 vs. 0.26±0.03) in ec-topic endometrial tissue of EMT group were significantly increased. The pain latency and serum PGE2 content [(214.31±19.52) ng/L vs. (423.78±35.61) ng/L] were significantly reduced (P<0.05). Compared with the EMT group, the number of body twists, serum PGF2αcontent and PGF2α/PGE2 ratio, apoptosis rate and protein expression levels of NLRP3, caspase-1, GSDMD, IL-1β, and IL-18 in rats in the Ningxin Huantong Tang-L group, Ningxin Huantong Tang-H group, and Gestrinone group were significantly reduced, while thepain latency and serum PGE2 content were significantly increased (P<0.05).Conclusion Ningxin Huantong Tang may exert a certain therapeutic effect on endometriosis dysmenorrhea rats by inhibiting NLRP3-mediated cellular pyroptosis, attenuating inflammatory re-sponse, and regulating the synthesis and release of PGE2 and PGF2α in serum. |
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