Zhang L, Zhao W, Zheng Z, Wang T, Zhao C, Zhou G, Jin H, Wang B
Department of Digestive Diseases, General Hospital, Tianjin Medical University, Tianjin, China.
Dis Esophagus. 2016 Oct;29(7):801-806. doi: 10.1111/dote.12385. Epub 2015 Aug 28.
The etiology of achalasia remains largely unknown. Considerable evidence reveals that the lower esophageal sphincter dysfunction is due to the lack of inhibitory neurotransmitter, secondary to esophageal neuronal inflammation or loss. Recent studies suggest hydrogen sulfide may act as an inhibitory transmitter in gastrointestinal tract, but study about hydrogen sulfide in human esophagus still lack. The aim of the study was to investigate if hydrogen sulfide synthesis enzymes could be detected in human esophagus and if the synthesis of the endogenous hydrogen sulfide could be affected in achalasia patients. Tissue samples in cardia, lower esophageal sphincter, 2 cm and 4 cm above lower esophageal sphincter were obtained from achalasia patients undergoing peroral endoscopic myotomy. Control tissues in lower esophageal sphincter were obtained from esophageal carcinoma patients. Expression of cystathionine-β-synthase and cystathionine-γ-lyase in lower esophageal sphincter of achalasia patients and control were detected by immunohistochemical staining. In addition, expression of cystathionine-β-synthase and cystathionine-γ-lyase were compared among different parts of esophagus in achalasia patients. Compared with control, the expression of cystathionine-β-synthase and cystathionine-γ-lyase in lower esophageal sphincter of achalasia patients was significantly reduced (χ = 11.429, P = 0.010). The expression of cystathionine-β-synthase and cystathionine-γ-lyase were lower in lower esophageal sphincter than that in 2 cm and 4 cm above lower esophageal sphincter, respectively (all P < 0.05). In conclusion, the expression of hydrogen sulfide synthesis enzymes, cystathionine-β-synthase and cystathionine-γ-lyase, can be detected in human esophagus and is reduced in patients with achalasia, which implicates the involvement of the two hydrogen sulfide synthesis enzymes in the pathophysiology of achalasia.
贲门失弛缓症的病因在很大程度上仍不清楚。大量证据表明，食管下括约肌功能障碍是由于缺乏抑制性神经递质，继发于食管神经元炎症或丧失。最近的研究表明，硫化氢可能作为胃肠道中的一种抑制性递质，但关于人食管中硫化氢的研究仍然缺乏。本研究的目的是调查人食管中是否能检测到硫化氢合成酶，以及贲门失弛缓症患者内源性硫化氢的合成是否会受到影响。从接受经口内镜下肌切开术的贲门失弛缓症患者中获取贲门、食管下括约肌、食管下括约肌上方2厘米和4厘米处的组织样本。食管下括约肌的对照组织取自食管癌患者。通过免疫组织化学染色检测贲门失弛缓症患者和对照者食管下括约肌中胱硫醚-β-合成酶和胱硫醚-γ-裂解酶的表达。此外，比较了贲门失弛缓症患者食管不同部位胱硫醚-β-合成酶和胱硫醚-γ-裂解酶的表达。与对照组相比，贲门失弛缓症患者食管下括约肌中胱硫醚-β-合成酶和胱硫醚-γ-裂解酶的表达明显降低（χ = 11.429，P = 0.010）。食管下括约肌中胱硫醚-β-合成酶和胱硫醚-γ-裂解酶的表达分别低于食管下括约肌上方2厘米和4厘米处（所有P < 0.05）。总之，人食管中可检测到硫化氢合成酶胱硫醚-β-合成酶和胱硫醚-γ-裂解酶的表达，且在贲门失弛缓症患者中降低，这表明这两种硫化氢合成酶参与了贲门失弛缓症的病理生理过程。
