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武汉市中医医院脾胃肝胆病科(消化内科),武汉 430050
副主任医师。研究方向:中医脾胃病。电话:027-84516759。E-mail:jmdcp4@163.com
主任医师。研究方向:中医肝胆病、脾胃病。E-mail:whlhw@126.com
收稿:2024-12-09,
修回:2025-04-17,
录用:2025-04-18,
纸质出版:2025-06-15
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夏鹏飞,金迪,梁金,等.香砂益胃汤对慢性萎缩性胃炎大鼠胃黏膜损伤的改善作用及机制 [J].中国药房,2025,36(11):1311-1316.
XIA Pengfei,JIN Di,LIANG Jin,et al.Improvement effects and mechanism of Xiangsha yiwei tang on gastric mucosal injury in rats with chronic atrophic gastritis[J].ZHONGGUO YAOFANG,2025,36(11):1311-1316.
夏鹏飞,金迪,梁金,等.香砂益胃汤对慢性萎缩性胃炎大鼠胃黏膜损伤的改善作用及机制 [J].中国药房,2025,36(11):1311-1316. DOI: 10.6039/j.issn.1001-0408.2025.11.04.
XIA Pengfei,JIN Di,LIANG Jin,et al.Improvement effects and mechanism of Xiangsha yiwei tang on gastric mucosal injury in rats with chronic atrophic gastritis[J].ZHONGGUO YAOFANG,2025,36(11):1311-1316. DOI: 10.6039/j.issn.1001-0408.2025.11.04.
目的
2
探讨香砂益胃汤对慢性萎缩性胃炎(CAG)大鼠胃黏膜损伤的改善作用及机制。
方法
2
将大鼠随机分为正常对照组,模型组,香砂益胃汤低、中、高剂量组(6、12、18 g/kg,以生药量计),香砂益胃汤高剂量+740 Y-P组[香砂益胃汤18 g/kg+转化生长因子β
1
(TGF-β
1
)/磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(Akt)通路激活剂740 Y-P 10 mg/kg
]
,每组18只。各组大鼠灌胃/注射相应药物,每天1次,连续4周。检测大鼠胃黏膜血流量、血清中胃激素[胃动素(MTL)、胃泌素(GAS)、胃蛋白酶(PP)
]
和炎症因子[肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)、IL-6
]
水平;观察大鼠胃黏膜组织病理形态;检测大鼠胃黏膜细胞凋亡率;检测大鼠胃黏膜组织中TGF-β
1
/PI3K/Akt信号通路相关蛋白和凋亡相关蛋白[B细胞淋巴瘤2(Bcl-2)、Bcl-2相关X蛋白(Bax)
]
的表达水平。
结果
2
与正常对照组比较,模型组大鼠胃黏膜组织结构异常,胃黏膜上皮细胞脱落,炎症细胞浸润明显;胃黏膜血流量,血清中MTL、GAS、PP水平,胃黏膜组织中Bcl-2蛋白表达水平均显著降低(
P
<0.05);血清中TNF-α、IL-1β、IL-6水平,细胞凋亡率,胃黏膜组织中Bax、TGF-β
1
蛋白表达水平和PI3K、Akt蛋白磷酸化水平均显著升高(
P
<0.05)。与模型组比较,香砂益胃汤各剂量组大鼠胃黏膜组织病理损伤减轻,炎症细胞浸润减少,上述定量指标均显著改善(
P
<0.05)。与香砂益胃汤高剂量组比较,香砂益胃汤高剂量+740 Y-P组大鼠胃黏膜病理损伤明显加重,上述定量指标均显著逆转(
P
<0.05)。
结论
2
香砂益胃汤可减轻CAG大鼠胃黏膜损伤,其作用机制与抑制TGF-β
1
/PI3K/Akt信号通路相关。
OBJECTIVE
2
To investigate the improvement effects and mechanism of Xiangsha yiwei tang on gastric mucosal injury in rats with chronic atrophic gastritis (CAG).
METHODS
2
Rats were randomly assigned into normal control group, model group, Xiangsha yiwei tang low-, medium- and high-dose groups (6, 12, 18 g/kg, calculated by crude drug), and high-dose group of Xiangsha yiwei tang+740 Y-P [Xiangsha yiwei tang 18 g/kg+transforming growth factor β
1
/phosphatidyl inositol 3 kinase/protein kinase B(TGF-β
1
/PI3K/Akt) pathway activator group 740 Y-P 10 mg/kg
]
, with 18 rats in each group. Rats in each group were administered the corresponding drugs via oral gavage or injection, once daily, for 4 consecutive weeks. Gastric mucosal blood flow, the levels of serum gastroint
estinal hormones [including motilin (MTL), gastrin (GAS), and pepsinogen (PP)
]
, as well as inflammatory cytokines [including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6
]
in rats were measured. Pathological damage to gastric mucosal tissue was observed in rats; the apoptotic rate of gastric mucosal cells was detected. The expressions of TGF-β
1
/PI3K/Akt signaling pathway-related proteins and apoptosis-related proteins [including B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax)
]
in the gastric mucosal tissues of rats were assessed.
RESULTS
2
Compared with normal control group, model group had abnormal gastric mucosal tissue structure, with shedding of gastric mucosal epithelial cells, and prominent infiltration of inflammatory cells. Gastric mucosal blood flow, the serum levels of MTL, GAS, PP, and Bcl-2 protein expression were lowered significantly, while serum levels of TNF-α, IL-1β and IL-6, apoptosis rate, protein expressions of Bax and TGF-β
1
, the phosphorylations of PI3K and Akt were increased significantly (
P
<0.05). Compared with model group, Xiangsha yiwei decoction groups exhibited attenuated histopathological injuries in gastric mucosal tissues, reduced inflammatory cell infiltration, and significant improvements in the aforementioned quantitative parameters (
P
<0.05). Compared with high-dose group of Xiangsha yiwei tang, high-dose group of Xiangsha yiwei decoction combined with 740 Y-P exhibited significantly aggravated histopathological injuries in gastric mucosal tissues, and the aforementioned quantitative parameters were markedly reversed (
P
<0.05).
CONCLUSIONS
2
Xiangsha yiwei tang can alleviate gastric mucosal damage in CAG rats, and its mechanism of action is related to the inhibition of TGF-β
1
/PI3K/Akt signaling pathway.
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