岭南急诊医学杂志
嶺南急診醫學雜誌
령남급진의학잡지
LINGNAN JOURNAL OF EMERGENCY MEDICINE
2015年
1期
36-38
,共3页
谢云%董晓亮%张伟%谢伟杰%姚友生
謝雲%董曉亮%張偉%謝偉傑%姚友生
사운%동효량%장위%사위걸%요우생
硫化氢%炔丙基甘氨酸%硫酸鱼精蛋白%间质性膀胱炎
硫化氫%炔丙基甘氨痠%硫痠魚精蛋白%間質性膀胱炎
류화경%결병기감안산%류산어정단백%간질성방광염
hydrogen sulfide%DL-propargylglycine%Protamine sulfate%interstitial cystitis
目的:探讨硫化氢(H2S)在硫酸鱼精蛋白(PS)诱导的大鼠慢性膀胱炎中的作用。方法:36只雌性 SD大鼠随机分为3组(每组12只),采用膀胱灌注 PS 构建慢性膀胱炎症大鼠模型,VonFrey 刷检测泌尿生殖区疼痛变化,尿流动力学检测膀胱功能。亚甲基蓝分光光度法测定膀胱中 H2S 含量,实时定量聚合酶链反应(RT-PCR)筛选H2S 各催化酶、P物质等mRNA 表达,Western blot 检测胱硫醚-γ-裂解酶(CSE)蛋白表达。结果:模型组大鼠膀胱中,其H2S 含量明显高于对照组(P <0.05)。大鼠膀胱中CSE的mRNA及蛋白水平表达升高(均P <0.05)。与对照组比较,模型组大鼠排尿间歇缩短,膀胱容量降低。而CSE抑制剂PAG 干预后其排尿间歇时间延长(390.79±41.62 vs 160.18±40.10, P <0.05),膀胱容量增加(0.99±0.11 vs 0.47±0.13, P <0.05)。此外,与模型组比较,PAG 组疼痛评分明显下降(P <0.05),P物质的mRNA 表达也下调(P <0.05)。结论:间质性膀胱炎时,膀胱组织中由 CSE 催化产生的内源性 H2S 水平明显增加,以 H2S 为靶点,抑制系统和组织中 H2S 生成可能可以改善IC/BPS 的尿频及疼痛情况。
目的:探討硫化氫(H2S)在硫痠魚精蛋白(PS)誘導的大鼠慢性膀胱炎中的作用。方法:36隻雌性 SD大鼠隨機分為3組(每組12隻),採用膀胱灌註 PS 構建慢性膀胱炎癥大鼠模型,VonFrey 刷檢測泌尿生殖區疼痛變化,尿流動力學檢測膀胱功能。亞甲基藍分光光度法測定膀胱中 H2S 含量,實時定量聚閤酶鏈反應(RT-PCR)篩選H2S 各催化酶、P物質等mRNA 錶達,Western blot 檢測胱硫醚-γ-裂解酶(CSE)蛋白錶達。結果:模型組大鼠膀胱中,其H2S 含量明顯高于對照組(P <0.05)。大鼠膀胱中CSE的mRNA及蛋白水平錶達升高(均P <0.05)。與對照組比較,模型組大鼠排尿間歇縮短,膀胱容量降低。而CSE抑製劑PAG 榦預後其排尿間歇時間延長(390.79±41.62 vs 160.18±40.10, P <0.05),膀胱容量增加(0.99±0.11 vs 0.47±0.13, P <0.05)。此外,與模型組比較,PAG 組疼痛評分明顯下降(P <0.05),P物質的mRNA 錶達也下調(P <0.05)。結論:間質性膀胱炎時,膀胱組織中由 CSE 催化產生的內源性 H2S 水平明顯增加,以 H2S 為靶點,抑製繫統和組織中 H2S 生成可能可以改善IC/BPS 的尿頻及疼痛情況。
목적:탐토류화경(H2S)재류산어정단백(PS)유도적대서만성방광염중적작용。방법:36지자성 SD대서수궤분위3조(매조12지),채용방광관주 PS 구건만성방광염증대서모형,VonFrey 쇄검측비뇨생식구동통변화,뇨류동역학검측방광공능。아갑기람분광광도법측정방광중 H2S 함량,실시정량취합매련반응(RT-PCR)사선H2S 각최화매、P물질등mRNA 표체,Western blot 검측광류미-γ-렬해매(CSE)단백표체。결과:모형조대서방광중,기H2S 함량명현고우대조조(P <0.05)。대서방광중CSE적mRNA급단백수평표체승고(균P <0.05)。여대조조비교,모형조대서배뇨간헐축단,방광용량강저。이CSE억제제PAG 간예후기배뇨간헐시간연장(390.79±41.62 vs 160.18±40.10, P <0.05),방광용량증가(0.99±0.11 vs 0.47±0.13, P <0.05)。차외,여모형조비교,PAG 조동통평분명현하강(P <0.05),P물질적mRNA 표체야하조(P <0.05)。결론:간질성방광염시,방광조직중유 CSE 최화산생적내원성 H2S 수평명현증가,이 H2S 위파점,억제계통화조직중 H2S 생성가능가이개선IC/BPS 적뇨빈급동통정황。
Objective: To investigate the effects of hydrogen sulfide (H2S) on protamine sulfate-induced chronic cystitis in rats. Methods: A total of 36 female Sprague-Dawley rats were randomized into 3 groups of 12. Chronic cystitis rat models were created by intravesical protamine sulfate. The changes of pain in urogenital area were detected by Von-Frey Hairs. Voiding pattern was investigated by cystometrography. The content of H2S in the bladder was measured by the colorimetry method. The mRNA levels of CSE, CBS, MST and substance P were analyzed with real time reverse transcription polymerase chain reaction. The protein levels of CSE were evaluated by Western blot. Results: In model group, the content of H2S in the bladder was obviously increased than that in the control group. Meanwhile, only the mRNA and protein levels of CSE increased significantly (both P < 0.05) among CSE,CBS and MST. Compared with control, the rats of model group showed decreased intercontraction intervals and bladder capacity. After administration of CSE antagonist PAG, both intercontraction intervals (390.79 ± 41.62 vs 160.18 ± 40.10, P <0.05) and bladder capacity (0.99±0.11 vs 0.47±0.13, P < 0.05)increased significantly. Furthermore, the PAG group showed significantly decreased pain score and substance P mRNA levels compared with the control group (both P <0.05). Conclusion: In interstital cystitis, endogenous H2S levels in the bladder are obviously increased by the catalysis of CSE. Therefore, inhibiting the production of H2S in the system and tissue may ameliorate the frequent micturition and the pain. H2S may act as a therapeutic target.