胃癌和癌前病变患者Cx32，Cx43表达与幽门螺杆菌感染的相关性

Relationship between Helicobacter pylori infection and expression of connexin （ Cx ）32 and Cx43 genes in gastric cancer and gastric precancerous lesions

目的探讨胃癌和癌前病变患者Cx32，Cx43表达改变与幽门螺杆菌（Hp）感染的关系。方法采用前瞻性成组设计方法将33例慢性浅表性胃炎（CSG）、88例癌前病变、70例胃癌患者，用快速尿素酶试验、碱性品红染色和14C尿素呼气试验检测Hp感染，PCR法检测Hp细胞毒相关蛋白A（CagA）基因，组织免疫化学链霉亲和素-生物素-过氧化物酶复合物（SABC）法检测胃黏膜Cx32，Cx43表达。结果胃癌组Cx32、Cx43阳性表达率分别为15．7％与32．9％，癌前病变组分别为51．1％与54．5％，均低于CSG组（100．0％VS93．9％，均P〈0．05）。胃癌患者Hp感染组Cx32阳性表达率为16．7％，与无Hp感染组（13．6％）比较差异无统计学意义；Cx43阳性表达率低于无Hp感染组（25％vs50％，P=0．039）。癌前病变患者Hp感染组Cx32、Cx43阳性表达率和表达强度均低于无Hp感染组（均P〈0．05）。Hp感染胃癌患者CagA^＋组Cx32阳性表达率与CagA^-组比较差异无统计学意义（12．8％VS33．3％，P=0．159）；Cx43阳性表达率低于CagA^-组（17．9％VS55．6％，P=0．027）。Hp感染CSG患者CagA^＋组与CagA^_组Cx32、Cx43阳性表达率均为100．0％，但CagA^＋组Cx43表达强度低于CagA^_组（P=0．032）。58例Hp感染癌前病变患者抗Hp治疗后48例Hp根除者Cx32、Cx43阳性表达率和表达强度均高于治疗前（均P〈0．05），而Hp未根除者与治疗前比较差异无统计学意义。结论胃癌和癌前病变Cx32，Cx43表达降低，其中Cx43表达降低与Hp感染，特别是与CagA^＋Hp感染有关，Hp根除可上调癌前病变患者Cx32，Cx43表达。

Objective To investigate the expression of connexin （Cx）32 and Cx43 genes in gastric cancer and precancerous lesion, and to investigate the relation between the changes of expression of Cx32 and Cx43 genes and Helicobacter pylori （Hp） infection. Methods Gastroscopy and biopsy of gastric mucosa were conducted on 33 patients with chronic superficial gastritis （ CSG）, 88 with precancerous lesion, and 70 with gastric cancer. Hp was detected by rapid urease test, basic fuchsin staining, and 14 C-urea breath test. The CagA gene of Hp was determined by PCR. SABC immunohistochemical method was used to detect the expression of Cx32 and Cx43 genes in gastric mucosa biopsy specimens. Results The positive expression rates of Cx32 and Cx43 genes were 15.7% and 32.9% respectively in the gastric cancer patients, 51.1% and 54.5% in the patients with precancerous lesion, and 100.0% and 93.9% in the CSG patients. The positive Cx32 and Cx43 expression rates of the gastric cancer and precancerous lesion patients were significantly lower than those of the CSG patients （ all P 〈 0.05 ）. The positive Cx32 expression rate of the gastric cancer patients with Hp infection was 16.7%, not significantly different from that of the gastric cancer patients without Hp infection （ 13.6% ）. The positive Cx43 expression rate of the gastric cancer patients with Hp infection was 25%, significantly lower than that of the gastric cancer patients without Hp infection （50%, P =0.039）. The positive Cx32 and Cx43 expression rates and expression intensity of the precancerous lesion patients with Hp infection were all significantly lower than those of the precancerous lesion patients without Hp infection（ all P 〈 0.05 ）. The positive Cx43 expression rate of the gastric cancer patients with CagA^＋ Hp infection was 17. 9%, significantly lower than that of the CagA^- Hp group （ 55.6% , P = 0.027 ）, however, the positive Cx32 expression rate of the gastric cancer patients with CagA ＋ Hp infection was 12.8%, not significantly different from that of the gastric cancer patients with CagA^- Hp infection （33.3%, P =0. 159）. The positive Cx32 and Cx43 expression rates of the CSG patients with CagA^＋ Hp and CagA^ - Hp infection were all 100%, but the expression intensity of the CagA^＋ Hp group was significantly lower than that of the CagA - Hp group （ P = 0. 032 ）. The positive Cx32 and Cx43 expression rates after Hp eradication of the precancerous lesion patients with Hp infection were 97.9% and 91.7% respectively, both significantly higher than those before eradication therapy （41. 4% and 44. 8% respectively, both P 〈 0.05 ）. However, the positive Cx32 and Cx43 expression rates of the precancerous lesion patients with Hp infection without Hp eradication were still 40% and 50%, not significantly different from those before treatment. Conclusion The expression levels of Cx32 and Cx43 in gastric cancer and precancerous lesion decrease. The change of expression of Cx43 was associated with Hp infection, especially CagA^＋ Hp infection. Hp eradication in patients with precancerous lesion up-regulates the expression of Cx32 and Cx43.