PDF(Pubmed)
Abstract：
UNASSIGNED: The Zuojin Pill (ZJP) is widely used for treating chronic atrophic gastritis (CAG) in clinical practice, effectively ameliorating symptoms such as vomiting, pain, and abdominal distension in patients. However, the underlying mechanisms of ZJP in treating CAG has not been fully elucidated.
UNASSIGNED: This study aimed to clarify the characteristic function of ZJP in the treatment of CAG and its potential mechanism.
UNASSIGNED: The CAG model was established by alternant administrations of ammonia solution and sodium deoxycholate, as well as an irregular diet. Therapeutic effects of ZJP on body weight, serum biochemical indexes and general condition were analyzed. HE staining and AB-PAS staining were analyzed to characterize the mucosal injury and the thickness of gastric mucosa. Furthermore, network pharmacology and molecular docking were used to predict the regulatory mechanism and main active components of ZJP in CAG treatment. RT-PCR, immunohistochemistry, immunofluorescence and Western blotting were used to measure the expression levels of apoptosis-related proteins, gastric mucosal barrier-associated proteins and PI3K/Akt signaling pathway proteins.
UNASSIGNED: The results demonstrated that ZJP significantly improved the general state of CAG rats, alleviated weight loss and gastric histological damage and reduced the serum biochemical indicators. Network pharmacology and molecular docking found that ZJP in treating CAG by inhibiting inflammation, suppressing apoptosis, and protecting the gastric mucosal barrier via the PI3K/Akt signaling pathway. Further experiments confirmed that ZJP obviously modulated the expression of key proteins involved in gastric mucosal cell apoptosis, such as Bax, Bad, Apaf-1, cleaved-caspase-3, cleaved-caspase-9, Cytochrome C, Bcl-2, and Bcl-xl. Moreover, ZJP significantly reversed the protein expression of Occludin, ZO-1, Claudin-4 and E-cadherin.
UNASSIGNED: Our study revealed that ZJP treats CAG by inhibiting the PI3K/Akt signaling pathway. This research provided a scientific basis for the rational use of ZJP in clinical practice.
UNASSIGNED: This study aimed to clarify the characteristic function of ZJP in the treatment of CAG and its potential mechanism.
UNASSIGNED: The CAG model was established by alternant administrations of ammonia solution and sodium deoxycholate, as well as an irregular diet. Therapeutic effects of ZJP on body weight, serum biochemical indexes and general condition were analyzed. HE staining and AB-PAS staining were analyzed to characterize the mucosal injury and the thickness of gastric mucosa. Furthermore, network pharmacology and molecular docking were used to predict the regulatory mechanism and main active components of ZJP in CAG treatment. RT-PCR, immunohistochemistry, immunofluorescence and Western blotting were used to measure the expression levels of apoptosis-related proteins, gastric mucosal barrier-associated proteins and PI3K/Akt signaling pathway proteins.
UNASSIGNED: The results demonstrated that ZJP significantly improved the general state of CAG rats, alleviated weight loss and gastric histological damage and reduced the serum biochemical indicators. Network pharmacology and molecular docking found that ZJP in treating CAG by inhibiting inflammation, suppressing apoptosis, and protecting the gastric mucosal barrier via the PI3K/Akt signaling pathway. Further experiments confirmed that ZJP obviously modulated the expression of key proteins involved in gastric mucosal cell apoptosis, such as Bax, Bad, Apaf-1, cleaved-caspase-3, cleaved-caspase-9, Cytochrome C, Bcl-2, and Bcl-xl. Moreover, ZJP significantly reversed the protein expression of Occludin, ZO-1, Claudin-4 and E-cadherin.
UNASSIGNED: Our study revealed that ZJP treats CAG by inhibiting the PI3K/Akt signaling pathway. This research provided a scientific basis for the rational use of ZJP in clinical practice.
摘要：
■左金丸（ZJP）在临床实践中被广泛用于治疗慢性萎缩性胃炎（CAG），有效改善呕吐等症状，疼痛,和腹胀患者。然而,ZJP治疗CAG的潜在机制尚未完全阐明.
■本研究旨在阐明ZJP在治疗CAG中的特征性功能及其潜在机制。
■通过氨溶液和脱氧胆酸钠交替给药建立CAG模型，以及不规律的饮食。ZJP对体重的治疗作用，分析血清生化指标和一般情况。分析HE染色和AB-PAS染色以表征粘膜损伤和胃粘膜厚度。此外，采用网络药理学和分子对接技术预测ZJP在CAG治疗中的调控机制和主要活性成分。RT-PCR,免疫组织化学，免疫荧光法和免疫印迹法检测细胞凋亡相关蛋白的表达水平,胃粘膜屏障相关蛋白和PI3K/Akt信号通路蛋白。
■结果表明，ZJP明显改善了CAG大鼠的一般状态，减轻体重减轻和胃组织学损伤，降低血清生化指标。网络药理学和分子对接研究发现,ZJP通过抑制炎症,抑制细胞凋亡，并通过PI3K/Akt信号通路保护胃黏膜屏障。进一步的实验证实，ZJP明显调节了胃粘膜细胞凋亡的关键蛋白的表达，比如Bax,糟糕，Apaf-1，cleaved-caspase-3，cleaved-caspase-9，细胞色素C，Bcl-2和Bcl-xl。此外，ZJP显著逆转Occludin的蛋白表达,ZO-1、Claudin-4和E-cadherin。
■我们的研究表明，ZJP通过抑制PI3K/Akt信号通路治疗CAG。本研究为临床合理使用ZJP提供了科学依据。
■本研究旨在阐明ZJP在治疗CAG中的特征性功能及其潜在机制。
■通过氨溶液和脱氧胆酸钠交替给药建立CAG模型，以及不规律的饮食。ZJP对体重的治疗作用，分析血清生化指标和一般情况。分析HE染色和AB-PAS染色以表征粘膜损伤和胃粘膜厚度。此外，采用网络药理学和分子对接技术预测ZJP在CAG治疗中的调控机制和主要活性成分。RT-PCR,免疫组织化学，免疫荧光法和免疫印迹法检测细胞凋亡相关蛋白的表达水平,胃粘膜屏障相关蛋白和PI3K/Akt信号通路蛋白。
■结果表明，ZJP明显改善了CAG大鼠的一般状态，减轻体重减轻和胃组织学损伤，降低血清生化指标。网络药理学和分子对接研究发现,ZJP通过抑制炎症,抑制细胞凋亡，并通过PI3K/Akt信号通路保护胃黏膜屏障。进一步的实验证实，ZJP明显调节了胃粘膜细胞凋亡的关键蛋白的表达，比如Bax,糟糕，Apaf-1，cleaved-caspase-3，cleaved-caspase-9，细胞色素C，Bcl-2和Bcl-xl。此外，ZJP显著逆转Occludin的蛋白表达,ZO-1、Claudin-4和E-cadherin。
■我们的研究表明，ZJP通过抑制PI3K/Akt信号通路治疗CAG。本研究为临床合理使用ZJP提供了科学依据。
