Institute of Public Health, Gansu University of Chinese Medicine, Lanzhou, Gansu, People's Republic of China.
Department of Respiratory Medicine, Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou, Gansu, People's Republic of China.
Int J Chron Obstruct Pulmon Dis. 2024 Feb 22;19:489-500. doi: 10.2147/COPD.S445680. eCollection 2024.
Chronic obstructive pulmonary disease (COPD) is a chronic respiratory ailment influenced by a blend of genetic and environmental factors. Inflammatory response and an imbalance in oxidative-antioxidant mechanisms constitute the primary pathogenesis of COPD. Glutathione S-transferase P1(GSTP1) plays a pivotal role as an antioxidant enzyme in regulating oxidative-antioxidant responses in the pulmonary system. The activation of the NOD-like receptor thermal protein domain (NLRP3) inflammatory vesicle can trigger an inflammatory response. Several investigations have implicated GSTP1 and NLRP3 in the progression of COPD; nonetheless, there remains debate regarding this mechanism.
Employing a case-control study design, 312 individuals diagnosed with COPD and 314 healthy controls were recruited from Gansu Province to evaluate the correlation between GSTP1 (rs4147581C>G and rs1695A>G) and NLRP3 (rs3806265T>C and rs10754558G>C) polymorphisms and the susceptibility to COPD.
The presence of the GSTP1 rs4147581G allele substantially elevated the susceptibility to COPD (CGvs.CC:OR=3.11,95% CI=1.961-4.935, <0.001;GGvs.CC:OR=2.065,95% CI=1.273-3.350, =0.003; CG+GGvs.CC:OR=2.594,95% CI=1.718-3.916, <0.001). Similarly, the NLRP3rs3806265T allele significantly increased the susceptibility to COPD (TC:TT:OR=0.432,95% CI=0.296-0.630; TC+CCvs.TT:OR=2.132,95% CI=1.479-3.074, <0.001). However, no statistically significant association was discerned between the rs1695A>G and rs10754558G>C polymorphisms and COPD susceptibility (>0.05).
In summary, this study ascertained that the GSTP1 rs4147581C>G polymorphism is associated with increased COPD susceptibility, with the G allele elevating the risk of COPD. Similarly, the NLRP3 rs3806265T>C polymorphism is linked to elevated COPD susceptibility, with the T allele heightening the risk of COPD.
慢性阻塞性肺疾病(COPD)是一种受遗传和环境因素综合影响的慢性呼吸道疾病。炎症反应和氧化-抗氧化机制失衡是 COPD 的主要发病机制。谷胱甘肽 S-转移酶 P1(GSTP1)作为一种抗氧化酶,在调节肺部的氧化-抗氧化反应中发挥着关键作用。NOD 样受体热蛋白结构域(NLRP3)炎性囊泡的激活可以引发炎症反应。多项研究表明 GSTP1 和 NLRP3 参与了 COPD 的进展;然而,关于这种机制仍存在争议。
采用病例对照研究设计,从甘肃省招募了 312 名 COPD 患者和 314 名健康对照者,评估 GSTP1(rs4147581C>G 和 rs1695A>G)和 NLRP3(rs3806265T>C 和 rs10754558G>C)多态性与 COPD 易感性的相关性。
GSTP1 rs4147581G 等位基因的存在显著增加了 COPD 的易感性(CG 对 CC:OR=3.11,95%CI=1.961-4.935,<0.001;GG 对 CC:OR=2.065,95%CI=1.273-3.350,=0.003;CG+GG 对 CC:OR=2.594,95%CI=1.718-3.916,<0.001)。同样,NLRP3 rs3806265T 等位基因显著增加了 COPD 的易感性(TC:TT:OR=0.432,95%CI=0.296-0.630;TC+CC 对 TT:OR=2.132,95%CI=1.479-3.074,<0.001)。然而,rs1695A>G 和 rs10754558G>C 多态性与 COPD 易感性之间没有发现统计学上的显著关联(>0.05)。
综上所述,本研究证实 GSTP1 rs4147581C>G 多态性与 COPD 易感性增加有关,G 等位基因增加了 COPD 的发病风险。同样,NLRP3 rs3806265T>C 多态性与 COPD 易感性增加有关,T 等位基因增加了 COPD 的发病风险。