The role of hydrogen sulfide(H_2S) in portal hypertension(PH)-induced esophagus-gastric junction vascular lesions in rabbits was observed. The rabbit PH models were established. The animals were randomly divided into the following groups: normal, PH, PH+sodium hydrosulfide(PH+S), PH+propargylglycine(PH+PPG). The plasma H_2S levels, apoptosis of esophageal-gastric junction vascular smooth muscle cells, and the expression of nuclear transcription factor-κB(NF-κB), p-AKT, IκBa and Bcl-2 were detected. The cystathionine γ lyase(cystathionine-gamma-splitting enzyme, CSE) in the junction vascular tissue was measured. The results showed that the plasma H_2S levels and the CSE expression levels had statistically significant difference among different groups(P<0.05). As compared with PH group, plasma H_2S levels were declined obviously(11.9±4.2 vs. 20.6±4.5, P<0.05), and CSE expression levels in the junction vascular tissue were notably reduced(1.7±0.6 vs. 2.8±0.8, P<0.05), apoptosis rate of vascular smooth muscle cells per unit area was significantly decreased(0.10±0.15 vs. 0.24±0.07, P<0.05), and the expression levels of p-AKT and NF-κB were significantly decreased(2.31±0.33 vs. 3.04±0.38, P<0.05; 0.33±0.17 vs. 0.51±0.23, P<0.05), however, IκBa and Bcl-2 expression increased obviously(5.57±0.17 vs. 3.67±0.13, P<0.05; 0.79±0.29 vs. 0.44±0.36, P<0.05) in PH+PPG group. As compared with PH group, H_2S levels were notably increased(32.7±7.3 vs. 20.6±4.5, P<0.05), the CSE levels in the junction vascular tissue were significantly increased(6.3±0.7 vs. 2.8±0.8, P<0.05), apoptosis rate of vascular smooth muscle cells per unit area was significantly increased(0.35±0.14 vs. 0.24±0.07, P<0.05), and the expression levels of p-AKT and NF-κB were significantly increased(4.29±0.49 vs. 3.04±0.38, P<0.05; 0.77±0.27 vs. 0.51±0.23, P<0.05), yet IκBa and Bcl-2 expression decreased significantly(3.23±0.24 vs. 3.67±0.13, P<0.05; 0.31±0.23 vs. 0.48±0.34, P<0.05) in PH+S group. It is concluded that esophagus-gastric junction vascular lesions happen under PH, and apoptosis of smooth muscle cells is declined. H_2S can activate NF-κB by the p-AKT pathway, leading to the down-regulation of Bcl-2, eventually stimulating apoptosis of vascular smooth muscle cells, easing PH. H_2S/CSE system may play an important role in remission of PH via the AKT-NF-κB pathway. The role of hydrogen sulfide (H_2S) in portal hypertension (PH) -induced esophagus-gastric junction vascular lesions in rabbits was observed. The rabbit PH models were established. The animals were randomly divided into the following groups: normal, PH, PH + The plasma H 2 S levels, apoptosis of esophageal-gastric junction vascular smooth muscle cells, and the expression of nuclear transcription factor-κB (NF-κB), p-sodium hydrosulfide (PH + S) The cystathionine γ lyase (cystathionine-gamma-splitting enzyme, CSE) in the junction vascular tissue was measured. The results showed that the plasma H_2S levels and the CSE expression levels had statistically significant difference among different groups (P <0.05). As compared with PH group, plasma H2S levels were significantly decreased (11.9 ± 4.2 vs. 20.6 ± 4.5, P <0.05), and CSE expression levels in the junction vascular tissue were not reduced reduced 0.6 vs. 2.8 ± 0.8, P <0.05), apoptosis ra The expression levels of p-AKT and NF-κB were significantly decreased (2.31 ± 0.33 vs. 3.04 ± 0.07, P <0.05) 0.38, P <0.05; 0.33 ± 0.17 vs. 0.51 ± 0.23, P <0.05), whereas IκBa and Bcl-2 expression increased obviously (5.57 ± 0.17 vs. 3.67 ± 0.13, P <0.05; 0.79 ± 0.29 vs. 0.44 ± 0.36, P <0.05) in PH + PPG group. As compared with PH group, H 2 S levels were notably increased (32.7 ± 7.3 vs. 20.6 ± 4.5, P <0.05) (6.3 ± 0.7 vs. 2.8 ± 0.8, P <0.05), and the expression levels of p- AKT and NF-κB were significantly increased (4.29 ± 0.49 vs. 3.04 ± 0.38, P <0.05; 0.77 ± 0.27 vs. 0.51 ± 0.23, P <0.05), while IκB and Bcl- . 3.67 ± 0.13, P <0.05; 0.31 ± 0.23 vs. 0.48 ± 0.34, P <0.05 ) in PH + S group. It is concluded thaH_2S can activate NF-κB by the p-AKT pathway, leading to the down-regulation of Bcl-2, eventually stimulating apoptosis of vascular smooth muscle cells, easing PH. H_2S / CSE system may play an important role in remission of PH via the AKT-NF-κB pathway.