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李玉凤,陈亮亮,李学军.基于TGF-β1/Smad3通路探讨脾胃培源方对慢性萎缩性胃炎大鼠干预作用[J].湖南中医药大学学报英文版,2019,39(2):173-177.[Click to copy
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| 基于TGF-β1/Smad3通路探讨脾胃培源方对慢性萎缩性胃炎大鼠干预作用 |
| 李玉凤,陈亮亮,李学军 |
| (安徽中医药大学, 安徽 合肥 230038;安徽中医药大学第二附属医院, 安徽 合肥 230061) |
| 摘要: |
| 目的 观察脾胃培源方对慢性萎缩性胃炎（chronic atrophic gastritis，CAG）大鼠血清胃蛋白酶原I（pepsinogenI，PGⅠ）、胃蛋白酶原Ⅱ（pepsinogenⅡ，PGⅡ）、胃泌素（gastrin-17，G-17）水平的影响，通过研究转化生长因子β1（transforming growth factor-β1，TGF-β1）和Smad3蛋白在CAG大鼠胃组织中的表达，探讨TGF-β1/Smad3信号传导通路在CAG发病过程中的作用以及脾胃培源方的治疗机制。方法 选用SPF 级Wistar雄性大鼠100只，随机分为：空白对照组、模型组、维酶素组、脾胃培源方（高、中、低剂量）组，采用幽门弹簧植入术配合高盐热淀粉糊灌胃法制备CAG大鼠模型。造模成功后，各组予以相关干预，连续灌胃4周，4周后处死大鼠取血清及胃组织。通过HE染色观察大鼠胃组织病理学的改变，并采用Elisa法和Western blot法检测血清PGⅠ、PGⅡ、G-17水平及TGF-β1、Smad3蛋白表达。结果 与空白对照组比较，模型组血清PGⅠ、G-17水平及Smad3蛋白表达显著降低（P<0.05），TGF-β1蛋白表达明显上升（P<0.05）；与模型组比较，脾胃培源方组和维酶素组血清PGⅠ、G-17水平及Smad3蛋白表达明显上升（P<0.05），TGF-β1蛋白表达明显降低（P<0.05），血清PGⅡ均未见明显变化，差异无统计学意义（P>0.05）；维酶素组和脾胃培源方（高、中、低剂量组）4组间采取两两比较，差异无统计学意义（P>0.05）。结论 脾胃培源方能明显改善CAG大鼠的胃组织损伤，下调胃组织TGF-β1蛋白表达及上调Smad3蛋白的表达，说明TGF-β1/Smad3信号转导通路参与了CAG发病过程，脾胃培源方治疗CAG可能通过干预该通路的表达而实现。 |
| 关键词: 慢性萎缩性胃炎 胃蛋白酶原 转化生长因子β1 Smad3 脾胃培源方 |
| DOI：10.3969/j.issn.1674-070X.2019.02.006 |
| Received:June 13, 2018 |
| 基金项目:安徽中医药大学临床科研项目（2017fydz010） |
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| Intervention Effect of Piwei Peiyuan Decoction on Rats with Chronic Atrophic Gastritis: An Analysis Based on the TGF-β1/Smad3 Signaling Pathway |
| LI Yufeng,CHEN Liangliang,LI Xuejun |
| (Anhui University of Chinese Medicine, Hefei, Anhui 230038, China;The Second Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui 230061, China) |
| Abstract: |
| Objective To investigate the effect of Piwei Peiyuan Decoction on the serum levels of pepsinogen I (PG I), pepsinogen Ⅱ (PG Ⅱ), and gastrin-17 (G-17) in rats with chronic atrophic gastritis (CAG), as well as the role of the TGF-β1/Smad3 signaling pathway in the development of CAG and the therapeutic mechanism of Piwei Peiyuan Decoction based on the expression of transforming growth factor-β1 (TGF-β1) and Smad3 in gastric tissue. Methods A total of 100 specific pathogen-free male Wistar rats were randomly divided into blank control group, model group, vitacoenzyme group, and high-, middle-, and low-dose Piwei Peiyuan Decoction groups. A rat model of CAG was established by spring implantation at the pylorus and high-salt hot starch paste by gavage. After the model was successfully established, each group was given the corresponding treatment, and after 4 consecutive weeks of gavage, the rats were sacrificed to collect serum and gastric tissue. HE staining was performed to observe the pathological changes of gastric tissue, and ELISA and Western blot were used to measure the serum levels of PG I, PG Ⅱ, and G-17 and the protein expression of TGF-β1 and Smad3. Results Compared with the blank control group, the model group had significant reductions in the serum levels of PG I and G-17 and the protein expression of Smad3 (P<0.05) and a significant increase in the protein expression of TGF-β1 (P<0.05). Compared with the model group, the Piwei Peiyuan Decoction groups and the vitacoenzyme group had significant increases in the serum levels of PG I and G-17 and the protein expression of Smad3 (P<0.05) and a significant reduction in the protein expression of TGF-β1 (P<0.05). There was no significant change or difference in the serum level of PG Ⅱ (P>0.05). There were no significant differences in the above indices between any two of the vitacoenzyme group and the high-, middle-, and low-dose Piwei Peiyuan Decoction groups (P>0.05). Conclusion Piwei Peiyuan Decoction can significantly improve gastric injury, downregulate the protein expression of TGF-β1, and upregulate the protein expression of Smad3 in CAG rats, suggesting that the TGF-β1/Smad3 signaling pathway may be involved in the development of CAG. Piwei Peiyuan Decoction may be therapeutic against CAG by exerting an intervention effect on this signaling pathway. |
| Key words: chronic atrophic gastritis transforming growth factor-β1 Smad3 Piwei Peiyuan Decoction |
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