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三七总皂苷对慢性萎缩性胃炎大鼠胃黏膜损伤及炎症反应的影
响及机制
Δ
＊
#
喻 玉 ，石 容，赵 龙（西南医科大学附属中医医院脾胃风湿免疫病科，四川 泸州 646000）
中图分类号 R965；R285.5 文献标志码 A 文章编号 1001-0408（2026）08-1021-06
DOI 10.6039/j.issn.1001-0408.2026.08.09
摘 要 目的 基于干细胞因子（SCF）/干细胞因子受体（c-kit）信号通路探讨三七总皂苷（PNS）对慢性萎缩性胃炎（CAG）大鼠胃
黏膜损伤、炎症反应的影响及潜在机制。方法 取SD雄性大鼠，以N-甲基-N′-硝基-N-亚硝基胍灌胃诱导+不规律饮食的方式构建
CAG大鼠模型，并将造模成功的大鼠随机分为模型组（Model组），阳性对照-维酶素组（Positive组，250 mg/kg），PNS低、高剂量组
（PNS-L、PNS-H组，9、18 mg/kg），PNS高剂量+SCF/c-kit抑制剂组（PNS-H+ISCK03组，18 mg/kg+47 mg/kg），每组8只；另取健康大
鼠8只，作为对照组（Control组）。末次给药后，检测各组大鼠血清中胃泌素（GAS）、胃动素（MTL）水平和胰多肽（PP）活性，以及
胃黏膜组织中肿瘤坏死因子α（TNF-α）、白细胞介素10（IL-10）、IL-8水平；观察其胃黏膜组织病理变化及上皮细胞超微结构，并进
行胃黏膜萎缩评分；检测其胃黏膜组织细胞凋亡情况及增殖细胞核抗原（PCNA）、核因子κB p65（NF-κB p65）、SCF、c-kit蛋白的表
达情况。结果 与Control组比较，Model组大鼠胃黏膜组织炎症细胞浸润明显，大量上皮细胞脱落且超微结构受损严重；胃黏膜萎
缩评分、胃黏膜组织中TNF-α和IL-8水平、细胞凋亡率、NF-κB p65蛋白的表达均显著升高或上调；血清中GAS、MTL水平和PP活
性，胃黏膜组织中IL-10水平，以及PCNA、SCF蛋白的表达和c-kit蛋白的磷酸化水平均显著降低或下调（P＜0.05）。与Model组比
较，Positive、PNS-L、PNS-H组大鼠胃黏膜组织中上述病理改变均明显好转，各定量指标均显著改善，且PNS-H组的改善较PNS-L
组更显著（P＜0.05）；而ISCK03可显著逆转高剂量PNS对大鼠上述指标的改善作用（P＜0.05）。结论 PNS可通过减轻炎症反应、
促进胃黏膜修复，从而改善CAG大鼠胃黏膜损伤；上述作用可能与激活SCF/c-kit信号通路有关。
关键词 三七总皂苷；慢性萎缩性胃炎；胃黏膜损伤；炎症反应；SCF/c-kit信号通路
Effects of Panax notoginseng saponins on gastric mucosal injury and inflammatory response in rats with
chronic atrophic gastritis
YU Yu，SHI Rong，ZHAO Long（Dept. of Spleen-Stomach， Rheumatology and Immunology， the Affiliated
Traditional Chinese Medicine Hospital of Southwest Medical University， Sichuan Luzhou 646000， China）
ABSTRACT OBJECTIVE To investigate the effects and potential mechanism of Panax notoginseng saponins （PNS） on gastric
mucosal injury and inflammatory response in rats with chronic atrophic gastritis （CAG） via the stem cell factor（SCF）/cellular
tyrosine kinase receptor（c-kit） signaling pathway. METHODS Male SD rats were used to establish a CAG rat model through
intragastric administration of N-methyl-N′-nitro-N-nitrosoguanidine combined with an irregular diet. Successfully modeled rats were
randomly divided into a model group， positive control-vitacoenzyme group （Positive group， 250 mg/kg）， PNS low- and high-dose
groups （PNS-L and PNS-H groups， 9， 18 mg/kg）， and high-dose PNS+SCF/c-kit inhibitor group （PNS-H+ISCK03 group， 18
mg/kg+47 mg/kg）， with 8 rats in each group. Additionally， 8 healthy rats were selected as a control group. After the final
administration， the activities of serum gastrin （GAS）， motilin （MTL） and pancreatic polypeptide （PP）， as well as the levels of
tumor necrosis factor-α （TNF-α）， interleukin-10 （IL-10）， and IL-8 in gastric mucosal tissues， were measured in each group.
Pathological changes of the gastric mucosal and ultrastructure of the epithelial cells were observed， and gastric mucosal atrophy was
scored. Cell apoptosis in gastric mucosal tissues and the expressions of proliferating cell nuclear antigen （PCNA）， nuclear factor-
κB p65 （NF- κB p65）， SCF and c-kit were detected. RESULTS Compared with the control group， the model group showed
significantly increased inflammatory cell infiltration in the gastric mucosal， extensive epithelial cell detachment， severe
ultrastructural damage， and significantly elevated or up-regulated gastric mucosal atrophy score， TNF-α and IL-8 levels in gastric
mucosal， cell apoptosis rate， and NF-κB p65 protein expression. Meanwhile， serum levels of GAS and MTL， PP activity， the
level of IL-10 in gastric mucosal tissue， and protein expressions of PCNA and SCF， as well as the phosphorylation level of c-kit，
were significantly decreased or down-regulated （P＜0.05）. Compared with the model group， Positive， PNS-L and PNS-H groups
exhibited markedly improved pathological changes in the
Δ 基金项目 四川省中医药管理局科学技术研究专项课题（No.
gastric mucosal and significant amelioration of the quantitative
2024MS148）
＊第一作者 副主任医师。研究方向：脾胃消化内科以及风湿免疫 indicators， with the PNS-H group showing significantly better
疾病的临床诊断及治疗。E-mail：oe0h4k@163.com improvement than the PNS-L group （P＜0.05）. However，
# 通信作者 副主任医师，硕士。研究方向：脾胃消化内科以及风 ISCK03 significantly reversed the ameliorative effects of high-
湿免疫疾病的临床诊断及治疗。E-mail：zhaolong1982@163.com dose PNS on the above indicators in rats （P＜0.05）.
中国药房 2026年第37卷第8期 China Pharmacy 2026 Vol. 37 No. 8 · 1021 ·
