The Compound Gastritis Mixture-containing Serum Regulates Gastric Epithelial Cell Pyroptosis Mediated by the NLRP3/Caspase-1 Pathway through Crosstalk between the TLR4 and Sonic Hedgehog Signaling Pathways

doi:10.12114/j.issn.1007-9572.2025.0209

Chinese General Practice ›› 2026, Vol. 29 ›› Issue (32): 4768-4776.DOI: 10.12114/j.issn.1007-9572.2025.0209

• Article • Previous Articles Next Articles

The Compound Gastritis Mixture-containing Serum Regulates Gastric Epithelial Cell Pyroptosis Mediated by the NLRP3/Caspase-1 Pathway through Crosstalk between the TLR4 and Sonic Hedgehog Signaling Pathways

1. Department of Gastroenterology and Hepatobiliary Medicine, the Second Affiliated Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou 350003, China
2. Key Laboratory of Chinese Medicine Preparation of Medical Institutions in Fujian Province (Fujian University of Traditional Chinese Medicine), Fuzhou 350003, China
3. Department of Pharmacy, the Second Affiliated Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou 350003, China

Received:2025-06-02 Revised:2025-08-20 Published:2026-11-15 Online:2026-10-10
Contact: HUANG Minghan
About author:
LIN Cuili and HE Youcheng are co-first authors

复方胃炎合剂含药血清通过Toll样受体4与Sonic Hedgehog通路串话调控NLRP3/Caspase-1通路介导胃黏膜上皮细胞焦亡研究

1．350003　福建省福州市，福建中医药大学附属第二人民医院脾胃肝胆科
2．350003　福建省福州市，福建省医疗机构中药制剂重点实验室（福建中医药大学）
3．350003　福建省福州市，福建中医药大学附属第二人民医院药学部

通讯作者: 黄铭涵
作者简介:
林翠丽和何友成为共同第一作者
作者贡献：
林翠丽负责实验方案的设计与优化，主导细胞与分子实验的实施，撰写论文；何友成共同负责实验设计与优化，共同撰写论文；王鑫负责中药制剂的制备，协助实验数据整理；林诗锦、郑泽宇负责数据分析；罗邦水、倪艺婧负责论文的修订；黄铭涵负责文章的质量控制与审查，统筹论文的最终定稿。
基金资助:
国家自然科学基金资助项目(82174365); 福建省中医药科技项目(2025ZDA002)

Abstract

Abstract:

Background

Chronic atrophic gastritis (CAG) is an important pathological stage in the progression from gastric mucosal inflammation to cancer. The TLR4 and Sonic Hedgehog (Shh) pathways play key roles in gastric mucosal injury and repair, while the NLRP3/Caspase-1 pathway is also involved in the inflammatory response and pyroptosis of gastric mucosal epithelial cells. The compound gastric inflammation mixture (CGM) has shown significant efficacy in the treatment of CAG, but its specific mechanism of action remains unclear.

Objective

To observe the effects of CGM-containing serum on pyroptosis of gastric mucosal epithelial cells by modulating the NLRP3/Caspase-1 pathway through the crosstalk between TLR4 and Shh signaling pathways, thereby exploring the potential mechanisms by which CGM treats CAG.

Methods

From January 2024 to March 2025, sixteen Wistar rats were randomly divided into a blank group and a CGM group, with 8 rats in each group. The blank group received intragastric administration of 0.9% sodium chloride solution. After continuous intragastric administration of CGM suspension for 10 days, serum was collected from the CGM group. The CCK-8 method was used to screen the CGM-containing serum, determining the optimal intervention concentration to be 10% and the optimal intervention time to be 48 hours. An ethanol-induced cell model was established to mimic CAG in human gastric mucosal epithelial cells. Cells that successfully underwent modeling were divided into model, CGM, TLR4 inhibitor, TLR4 inhibitor+CGM, TLR4 agonist, TLR4 agonist+CGM, Shh inhibitor, Shh inhibitor+CGM, Shh agonist, and Shh agonist+CGM groups. Meanwhile, normal GES-1 cells with normal rat serum were used as the blank group. The mRNA and protein expression levels of TLR4, NF-κB, Shh, NLRP3, and Caspase-1 were detected using RT-qPCR and Western blotting, while the levels of interleukin (IL) -1β, IL-6, and IL-18 in cell supernatants were measured using enzyme-linked immunosorbent assay (ELISA).

Results

Compared to the blank group, the model group exhibited increased mRNA and protein levels of TLR4, NF-κB, NLRP3, and Caspase-1, along with decreased mRNA and protein levels of Shh (P<0.05). The levels of IL-1β, IL-6, and IL-18 in the cell supernatants were significantly elevated (P<0.05). Compared to the model group, the CGM group, TLR4 inhibitor group, and Shh agonist group showed decreased mRNA levels of TLR4, NF-κB, NLRP3, and Caspase-1, while Shh mRNA levels were elevated (P<0.05). The CGM group also demonstrated decreased protein expression levels of NF-κB, NLRP3, and Caspase-1 (P<0.05). The TLR4 inhibitor group showed reduced protein expression of TLR4, NF-κB, NLRP3, and Caspase-1 and increased Shh protein expression (P<0.05). In the TLR4 agonist group, TLR4 protein expression was elevated (P<0.05). The Shh inhibitor group exhibited increased protein levels of TLR4 and NF-κB (P<0.05). The Shh agonist group showed decreased protein expression of NF-κB, NLRP3, and Caspase-1, alongside increased Shh protein expression (P<0.05). The levels of IL-1β, IL-6, and IL-18 in the cell supernatants were significantly reduced in the CGM group (P<0.05). The TLR4 inhibitor group and Shh agonist group had decreased IL-1β levels in the cell supernatants (P<0.05), while the TLR4 agonist group and Shh inhibitor group showed increased IL-1β levels (P<0.05). Compared to the CGM group, the TLR4 inhibitor + CGM group exhibited decreased mRNA levels of TLR4 and Caspase-1, along with reduced mRNA and protein expression levels of NF-κB and NLRP3, and increased mRNA and protein expression levels of Shh (P<0.05). In the TLR4 agonist+CGM group, mRNA levels of TLR4 and NF-κB were elevated, while Shh mRNA expression decreased (P<0.05). The Shh inhibitor+CGM group showed decreased Shh mRNA levels (P<0.05). In the Shh agonist+CGM group, mRNA and protein expression levels of TLR4, NF-κB, and Caspase-1 were reduced, while Shh mRNA and protein expression levels were increased (P<0.05). Both the TLR4 agonist + CGM group and Shh inhibitor + CGM group demonstrated elevated serum levels of IL-1β, IL-6, and IL-18 (P<0.05).

Conclusion

CGM-containing serum may regulate the NLRP3/Caspase-1 pathway and mediate the pyroptosis process of gastric epithelial cells by influencing the crosstalk between the TLR4 and Shh pathways, thereby improving the inflammatory-cancer transformation process in ethanol-induced GES-1 cells and exerting therapeutic effects on CAG.

Key words: Chronic atrophic gastritis, Compound gastritis mixture, NLRP3/Caspase-1 pathway, Pyroptosis

摘要：

背景

慢性萎缩性胃炎（CAG）是胃黏膜"炎-癌"转化的重要病理阶段，Toll样受体4（TLR4）与Sonic Hedgehog（Shh）通路在胃黏膜损伤与修复中起关键作用，NLRP3/Caspase-1通路亦参与胃黏膜上皮细胞的炎症反应和焦亡过程。复方胃炎合剂（CGM）在CAG治疗中效果显著，但其具体作用机制尚不清楚。

目的

观察CGM含药血清通过TLR4与Shh信号通路串话调控NLRP3/Caspase-1通路对胃黏膜上皮细胞焦亡的影响，探讨CGM治疗CAG可能的作用机制。

方法

于2024年1月—2025年3月，将16只Wistar大鼠随机分为空白组和CGM组，每组8只。空白组接受0.9%氯化钠溶液灌胃，CGM组以CGM混悬液连续灌胃10 d后采集血清。采用CCK-8法筛选CGM含药血清，测得最佳干预浓度为10%，最佳干预时间为48 h。采用乙醇诱导人胃黏膜上皮细胞建立CAG细胞模型。将造模成功细胞分为模型组、CGM组、TLR4抑制剂组、TLR4抑制剂+CGM组、TLR4激动剂组、TLR4激动剂+CGM组、Shh抑制剂组、Shh抑制剂+CGM组、Shh激动剂组、Shh激动剂+CGM组。同时将正常GES-1+正常大鼠血清作为空白组。采用RT-qPCR和Western blotting法分别检测细胞TLR4、NF-κB、Shh、NLRP3、Caspase-1 mRNA与蛋白表达，采用酶联免疫吸附试验（ELISA）法检测细胞上清液中白介素（IL）-1β、IL-6、IL-18水平。

结果

与空白组比较，模型组细胞TLR4、NF-κB、NLRP3、Caspase-1 mRNA与蛋白表达均升高，Shh mRNA与蛋白表达下降，细胞上清液中IL-1β、IL-6、IL-18水平均升高（P<0.05）。与模型组相比，CGM组、TLR4抑制组与Shh激动组TLR4、NF-κB、NLRP3、Caspase-1 mRNA水平均下降，Shh mRNA水平升高（P<0.05）；CGM组NF-κB、NLRP3、Caspase-1蛋白表达均下降（P<0.05）；TLR4抑制组TLR4、NF-κB、NLRP3、Caspase-1蛋白表达均下降，Shh蛋白表达上升（P<0.05）；TLR4激动剂组TLR4蛋白表达升高（P<0.05）；Shh抑制剂组TLR4、NF-κB蛋白表达升高（P<0.05）；Shh激动剂组NF-κB、NLRP3、Caspase-1蛋白表达均下降，Shh蛋白表达升高（P<0.05）；CGM组细胞上清液中IL-1β、IL-6、IL-18水平均降低（P<0.05）；TLR4抑制剂组与Shh激动剂组细胞上清中IL-1β水平均下降（P<0.05），TLR4激动剂组、Shh抑制剂组IL-1β水平升高（P<0.05）。与CGM组相比，TLR4抑制剂+CGM组TLR4、Caspase-1 mRNA水平下降，NF-κB、NLRP3 mRNA与蛋白表达下降，Shh mRNA与蛋白表达升高（P<0.05）；TLR4激动剂+CGM组TLR4、NF-κB mRNA水平升高，Shh mRNA表达下降（P<0.05）；Shh抑制剂+CGM组Shh mRNA水平下降（P<0.05）；Shh激动剂+CGM组TLR4、NF-κB、Caspase-1 mRNA与蛋白表达下降，Shh mRNA与蛋白表达升高（P<0.05）；TLR4激动剂+CGM组和Shh抑制剂+CGM组血清IL-1β、IL-6与IL-18均升高（P<0.05）。

结论

CGM含药血清可能通过影响TLR4与Shh通路串话调控NLRP3/Caspase-1通路介导胃上皮细胞焦亡过程，改善乙醇诱导GES-1细胞的炎-癌转化进程，从而发挥治疗CAG的作用。

关键词: 慢性萎缩性胃炎, 复方胃炎合剂, NLRP3/Caspase-1通路, 细胞焦亡

CLC Number:

R 573.22

LIN Cuili,HE Youcheng,HUANG Minghan, et al. The Compound Gastritis Mixture-containing Serum Regulates Gastric Epithelial Cell Pyroptosis Mediated by the NLRP3/Caspase-1 Pathway through Crosstalk between the TLR4 and Sonic Hedgehog Signaling Pathways[J]. Chinese General Practice, 2026, 29(32): 4768-4776. DOI: 10.12114/j.issn.1007-9572.2025.0209.
林翠丽,何友成,黄铭涵等. 复方胃炎合剂含药血清通过Toll样受体4与Sonic Hedgehog通路串话调控NLRP3/Caspase-1通路介导胃黏膜上皮细胞焦亡研究[J]. 中国全科医学, 2026, 29(32): 4768-4776. DOI: 10.12114/j.issn.1007-9572.2025.0209.

Figures/Tables 8

References 28

[1]	Morgan D R, Corral J E, Li D, et al. ACG clinical guideline: diagnosis and management of gastric premalignant conditions[J]. Am J Gastroenterol, 2025, 120(4): 709-737. DOI: 10.14309/ajg.0000000000003350.
[2]	国家消化系疾病临床医学研究中心(上海)，国家消化道早癌防治中心联盟，中华医学会消化病学分会幽门螺杆菌学组, 等. 中国胃黏膜癌前状态和癌前病变的处理策略专家共识(2020年)[J]. 中华消化杂志, 2020, 40(11): 731-741.
[3]	胡嘉敏，孙宇杰，黄德斌. 半夏泻心汤激活Hippo/YAP信号通路减轻慢性萎缩性胃炎[J]. 中国药理学通报, 2025, 41(8): 1578-1583.
[4]	袁艳，杨烨，晏娇艳, 等. 基于网络药理学、微阵列数据分析和分子对接探索头花蓼治疗幽门螺杆菌相关性胃炎的分子机制[J]. 中国药理学通报, 2023, 39(5): 961-969.
[5]	黄铭涵，黄健，李思汉, 等. 复方胃炎合剂逆转胃癌前病变的临床研究[J]. 中国中医药信息杂志, 2016, 23(4): 20-23.
[6]	Zhang T Q, Zhang K P, Ji K Y, et al. microRNA-365 inhibits YAP through TLR4-mediated IRF3 phosphorylation and thereby alleviates gastric precancerous lesions[J]. Cancer Cell Int, 2020, 20(1): 549.
[7]	Zhou P, Zheng Z H, Wan T, et al. Yiqi Jiedu Huayu decoction inhibits precancerous lesions of chronic atrophic gastritis by inhibiting NLRP3 inflammasome-mediated pyroptosis[J]. World J Gastrointest Oncol, 2024, 16(7): 3158-3168. DOI: 10.4251/wjgo.v16.i7.3158.
[8]	Tu W L, Hong Y J, Huang M A, et al. Effect of kaempferol on hedgehog signaling pathway in rats with—chronic atrophic gastritis -based on network pharmacological screening and experimental verification[J]. Biomed Pharmacother, 2022, 145: 112451. DOI: 10.1016/j.biopha.2021.112451.
[9]	Ding L, Sontz E A, Saqui-Salces M, et al. Interleukin-1β suppresses gastrin via primary cilia and induces antral hyperplasia[J]. Cell Mol Gastroenterol Hepatol, 2021, 11(5): 1251-1266. DOI: 10.1016/j.jcmgh.2020.12.008.
[10]	Han L P, Li T, Wang Y Y, et al. Weierning, a Chinese patent medicine, improves chronic atrophic gastritis with intestinal Metaplasia[J]. J Ethnopharmacol, 2023, 309: 116345. DOI: 10.1016/j.jep.2023.116345.
[11]	Zhou Z H, Hu C, Cui B, et al. Ginsenoside Rg1 suppresses pyroptosis via the NF-κB/NLRP3/GSDMD pathway to alleviate chronic atrophic gastritis in vitro and in vivo[J]. J Agric Food Chem, 2024. DOI: 10.1021/acs.jafc.4c01271.
[12]	Xiao S L, Shen Y C, Zhang M L, et al. VacA promotes pyroptosis via TNFAIP3/TRAF1 signaling to induce onset of atrophic gastritis[J]. Microbiol Res, 2025, 296: 128142. DOI: 10.1016/j.micres.2025.128142.
[13]	黄铭涵，李思汉，田琳, 等. 基于Sonic Hedgehog通路探讨复方胃炎合剂干预慢性萎缩性胃炎癌前病变的机制[J]. 湖南中医药大学学报, 2021, 41(2): 230-235. DOI: 10.3969/j.issn.1674-070X.2021.02.013.
[14]	李思汉，林秀明，田琳, 等. 健脾清化舒络中药对慢性萎缩性胃炎大鼠Sonic Hedgehog信号通路的影响[J]. 北京中医药大学学报, 2021, 44(2): 143-151.
[15]	何瑞坤，黄焕迪，戴庆玲, 等. 高良姜、红豆蔻及大高良姜的挥发油对乙醇致GES-1细胞损伤的保护作用及机制研究[J]. 中华中医药学刊, 2022, 40(6): 81-85, 277.
[16]	包雨晴. 基于大黄黄连泻心汤逆转GES-1细胞损伤探讨其煎服方法[D]. 南京: 南京中医药大学, 2018.
[17]	钱荣，安佳鑫，续晓琪, 等. 黑果枸杞多糖结构表征及对乙醇诱导胃黏膜上皮细胞损伤的影响[J]. 食品科学, 2024, 45(9): 109-115.
[18]	刘晓萌，杨倩，郎晓猛, 等. 基于网络药理学及实验验证探讨加味当归芍药散治疗慢性萎缩性胃炎的机制[J]. 中国药理学通报, 2023, 39(3): 560-568.
[19]	杨春波，周维湛，张恩平, 等. 中医辨证分型治疗慢性萎缩性胃炎疗效总结[J]. 中医杂志, 1988, 29(10): 34-37.
[20]	Burgueño J F, Fritsch J, González E E, et al. Epithelial TLR4 signaling activates DUOX2 to induce microbiota-driven tumorigenesis[J]. Gastroenterology, 2021, 160(3): 797-808.e6. DOI: 10.1053/j.gastro.2020.10.031.
[21]	Kim Y C, Lee S E, Kim S K, et al. Toll-like receptor mediated inflammation requires FASN-dependent MYD88 palmitoylation[J]. Nat Chem Biol, 2019, 15(9): 907-916.
[22]	黄铭涵，黄健，陈琴, 等. 健脾清化中药复方对大鼠慢性萎缩性胃炎TLR4-MyD88依赖途径蛋白表达及TNF-α的影响[J]. 中国药理学通报, 2016, 32(9): 1321-1325. DOI: 10.3969/j.issn.1001-1978.2016.09.026.
[23]	李思汉，黄铭涵，黄健, 等. 健脾清化中药复方对慢性萎缩性胃炎大鼠TLR4/NF-κB/COX-2信号通路的影响[J]. 中国中西医结合消化杂志, 2016, 24(7): 504-508.
[24]	Li S H, Huang M H, Chen Q, et al. Confirming the effects of qinghuayin against chronic atrophic gastritis and a preliminary observation of the involved inflammatory signaling pathways: an in vivo study[J]. Evid Based Complement Alternat Med, 2018, 2018: 4905089. DOI: 10.1155/2018/4905089.
[25]	Fu J N, Wu H. Structural mechanisms of NLRP3 inflammasome assembly and activation[J]. Annu Rev Immunol, 2023, 41: 301-316. DOI: 10.1146/annurev-immunol-081022-021207.
[26]	Yu P, Zhang X, Liu N, et al. Pyroptosis: mechanisms and diseases[J]. Signal Transduct Target Ther, 2021, 6(1): 128. DOI: 10.1038/s41392-021-00507-5.
[27]	Rao Z P, Zhu Y T, Yang P, et al. Pyroptosis in inflammatory diseases and cancer[J]. Theranostics, 2022, 12(9): 4310-4329. DOI: 10.7150/thno.71086.
[28]	Huang Y, Xu W, Zhou R B. NLRP3 inflammasome activation and cell death[J]. Cell Mol Immunol, 2021, 18(9): 2114-2127. DOI: 10.1038/s41423-021-00740-6.

引物名称	引物序列（5'-3'）	产物长度（bp）
TLR4		138
Forward	ACCTGTCCCTGAACCCTATGAA
Reverse	CTTCTAAACCAGCCAGACCTTG
NF-κB		180
Forward	AGTGTGGAGGCTGCCTTGCGAATG
Reverse	TGGGCTTTCAAGACTGGAACGGTC
Shh		211
Forward	ACCGAGGGCTGGGACGAAGA
Reverse	ATTTGGCCGCCACCGAGTT
NLRP3		93
Forward	GTGGTGACCCTCTGTGAGGT
Reverse	TCTTCCTGGAGCGCTTCTAA
Caspase-1		120
Forward	ACGCCTTGCCCTCATAAT
Reverse	TCTAATACATCTGGGACTTCTT
GAPDH		240
Forward	GTTGGAGGTCGGAGTCAACGGA
Reverse	GAGGGATCTCGCTCCTGGAGGA

引物名称	引物序列（5'-3'）	产物长度（bp）
TLR4		138
Forward	ACCTGTCCCTGAACCCTATGAA
Reverse	CTTCTAAACCAGCCAGACCTTG
NF-κB		180
Forward	AGTGTGGAGGCTGCCTTGCGAATG
Reverse	TGGGCTTTCAAGACTGGAACGGTC
Shh		211
Forward	ACCGAGGGCTGGGACGAAGA
Reverse	ATTTGGCCGCCACCGAGTT
NLRP3		93
Forward	GTGGTGACCCTCTGTGAGGT
Reverse	TCTTCCTGGAGCGCTTCTAA
Caspase-1		120
Forward	ACGCCTTGCCCTCATAAT
Reverse	TCTAATACATCTGGGACTTCTT
GAPDH		240
Forward	GTTGGAGGTCGGAGTCAACGGA
Reverse	GAGGGATCTCGCTCCTGGAGGA

乙醇浓度	原始吸光度值（OD值）
乙醇浓度	1 h	2 h	4 h	6 h	8 h
0	0.977±0.034	0.937±0.036	0.957±0.032	0.972±0.013	0.968±0.013
200 mmol/L	0.935±0.029	0.795±0.033	0.667±0.038^a	0.663±0.049^a	0.532±0.057^a
400 mmol/L	0.889±0.013	0.733±0.046	0.591±0.039^a	0.561±0.052^a	0.452±0.060^a
600 mmol/L	0.906±0.010	0.555±0.042^a	0.499±0.013^a	0.418±0.014^a	0.375±0.044^a
800 mmol/L	0.858±0.037	0.509±0.014^a	0.347±0.047^a	0.247±0.047^a	0.171±0.061^a
1 000 mmol/L	0.841±0.034	0.493±0.007^a	0.273±0.018^a	0.175±0.039^a	0.096±0.005^a
F值	9.46	89.08	162.10	167.60	136.40
P值	<0.001	<0.001	<0.001	<0.001	<0.001

乙醇浓度	原始吸光度值（OD值）
乙醇浓度	1 h	2 h	4 h	6 h	8 h
0	0.977±0.034	0.937±0.036	0.957±0.032	0.972±0.013	0.968±0.013
200 mmol/L	0.935±0.029	0.795±0.033	0.667±0.038^a	0.663±0.049^a	0.532±0.057^a
400 mmol/L	0.889±0.013	0.733±0.046	0.591±0.039^a	0.561±0.052^a	0.452±0.060^a
600 mmol/L	0.906±0.010	0.555±0.042^a	0.499±0.013^a	0.418±0.014^a	0.375±0.044^a
800 mmol/L	0.858±0.037	0.509±0.014^a	0.347±0.047^a	0.247±0.047^a	0.171±0.061^a
1 000 mmol/L	0.841±0.034	0.493±0.007^a	0.273±0.018^a	0.175±0.039^a	0.096±0.005^a
F值	9.46	89.08	162.10	167.60	136.40
P值	<0.001	<0.001	<0.001	<0.001	<0.001

CGM含药血清体积分数	细胞活力
CGM含药血清体积分数	12 h	24 h	48 h	72 h
0	100.000	100.000	100.000	100.000
1%	95.410±1.121	102.810±1.546	99.000±2.646	98.463±1.253
5%	102.217±1.644	106.913±1.601	112.693±1.943^a	101.593±1.640
10%	109.473±2.126^a	114.220±1.194^a	126.733±1.226^a	102.793±1.414
15%	106.797±1.569	109.133±2.316	124.283±1.096^a	103.557±2.338
20%	106.557±1.017	108.630±3.024	119.547±2.050^a	101.777±1.638
F值	40.65	21.70	146.80	4.34
P值	<0.001	<0.001	<0.001	0.017

The Compound Gastritis Mixture-containing Serum Regulates Gastric Epithelial Cell Pyroptosis Mediated by the NLRP3/Caspase-1 Pathway through Crosstalk between the TLR4 and Sonic Hedgehog Signaling Pathways

复方胃炎合剂含药血清通过Toll样受体4与Sonic Hedgehog通路串话调控NLRP3/Caspase-1通路介导胃黏膜上皮细胞焦亡研究

RichHTML

PDF

Knowledge

Abstract

Cite this article

share this article

Figures/Tables 8

References 28

Related Articles 5

Recommended Articles

Metrics

Comments

组别	细胞活力
空白组	100.000
空白血清组	99.123±0.198
CGM含药血清组	115.367±0.153^a
F值	73.50
P值	<0.001

组别	TLR4	NF-κB	Shh	NLRP3	Caspase-1
空白组	1.000	1.000	1.000	1.000	1.000
模型组	1.810±0.036^a	1.783±0.035^a	0.400±0.020^a	1.550±0.030^a	1.500±0.020^a
CGM组	1.200±0.020^b	1.300±0.020^b	0.700±0.020^b	1.250±0.020^b	1.350±0.020^b
TLR4抑制剂组	1.100±0.020^b	1.200±0.020^b	0.700±0.020^b	1.150±0.020^b	1.250±0.020^b
TLR4抑制剂+CGM组	0.950±0.020^c	0.900±0.020^c	0.850±0.020^c	0.850±0.020^c	0.750±0.020^c
TLR4激动剂组	1.900±0.020^b	1.850±0.030^b	0.300±0.020^b	1.650±0.030^b	1.600±0.020^b
TLR4激动剂+CGM组	1.400±0.020^c	1.500±0.020^c	0.550±0.020^c	1.300±0.020	1.450±0.020
Shh抑制剂组	1.300±0.020^b	1.400±0.020^b	0.250±0.020^b	1.150±0.020^b	1.350±0.020^b
Shh抑制剂+CGM组	1.150±0.020	1.250±0.020	0.320±0.020^c	1.100±0.020	1.200±0.020
Shh激动剂组	1.200±0.020^b	1.300±0.020^b	1.100±0.020^b	1.250±0.020^b	1.350±0.020^b
Shh激动剂+CGM组	1.100±0.020^c	1.200±0.020^c	1.050±0.020^c	1.150±0.020	1.250±0.020^c
F值	647.80	523.00	819.60	582.00	340.80
P值	<0.001	<0.001	<0.001	<0.001	<0.001

组别	TLR4	NF-κB	Shh	NLRP3	Caspase-1
空白组	1.080±0.230	0.983±0.015	0.993±0.012	1.030±0.061	0.997±0.006
模型组	1.730±0.208^a	1.797±0.176^a	0.333±0.153^a	1.800±0.100^a	1.863±0.148^a
CGM组	1.500±0.100	1.28±0.166^b	0.560±0.122	1.333±0.153^b	1.267±0.208^b
TLR4抑制剂组	0.900±0.200^b	0.693±0.253^b	0.800±0.100^b	0.467±0.115^b	0.567±0.208^b
TLR4抑制剂+CGM组	1.300±0.200	0.467±0.153^c	1.067±0.058^c	0.500±0.100	1.103±0.205^c
TLR4激动剂组	2.333±0.152^b	1.733±0.153	0.533±0.153	2.067±0.153	2.300±0.100
TLR4激动剂+CGM组	1.500±0.200	0.967±0.153	0.767±0.153	1.533±0.058	1.533±0.252
Shh抑制剂组	2.333±0.208^b	2.467±0.153^b	0.500±0.100	1.867±0.153	2.133±0.208
Shh抑制剂+CGM组	1.500±0.200	1.300±0.200	0.767±0.153	1.467±0.153	1.633±0.208
Shh激动剂组	1.233±0.251	0.900±0.100^b	1.133±0.208^b	1.033±0.115^b	1.400±0.200^b
Shh激动剂+CGM组	0.800±0.100^c	0.567±0.058^c	1.533±0.058^c	0.433±0.153	1.187±0.121^c
F值	20.89	44.63	22.08	27.28	66.20
P值	<0.001	<0.001	<0.001	<0.001	<0.001

组别	IL-1β	IL-6	IL-18
空白组	180.000±30.000	51.667±7.638	53.333±7.638
模型组	718.333±98.784^a	112.667±16.166^a	84.333±10.066^a
CGM组	109.000±11.000^b	31.667±7.638^b	32.000±2.646^b
TLR4抑制剂组	431.000±32.047^b	79.333±10.504	86.000±8.888
TLR4抑制剂+CGM组	263.333±61.101	113.333±15.275	67.333±11.930
TLR4激动剂组	948.333±54.151^b	126.667±20.817	102.667±6.429
TLR4激动剂+CGM组	390.333±36.474^c	103.333±15.275^c	79.000±10.536^c
Shh抑制剂组	1 008.333±85.781^b	126.667±20.817	107.333±3.786
Shh抑制剂+CGM组	668.000±77.485^c	72.667±5.508^c	64.667±7.371^c
Shh激动剂组	403.667±77.087^b	101.000±11.533	85.667±9.074
Shh激动剂+CGM组	266.333±60.335	88.333±16.073	54.000±6.245
F值	71.49	13.69	22.89
P值	<0.001	<0.001	<0.001

[1]	SHI Zhiyao, GAO Yu, LIU Likun, GUO Zhi, WANG Xixing. Research Progress on Cell Pyroptosis in Colorectal Cancer Transformation and Disease Development [J]. Chinese General Practice, 2026, 29(27): 4026-4032.
[2]	HE Linqin, LI Xiaodong, LIU Hongpeng, CHEN Qipeng, TANG Zonghan, REN Xaingqian, SONG Hanbing. Acupotomy Inhibits Knee Osteoarthritis Through Activating A3AR to Suppress Chondrocyte Pyroptosis Via the Wnt/β-catenin Signaling Pathway [J]. Chinese General Practice, 2026, 29(15): 2056-2066.
[3]	WANG Ting, WANG Haiyan, FU Wenjun. Effect of Chronic Atrophic Gastritis Treated with Different Acupuncture and Moxibustion Therapies: a Network Meta-analysis [J]. Chinese General Practice, 2024, 27(23): 2913-2920.
[4]	LI Jiawu, QIN Feng, SONG Shengqin, ZHAI Tin, XIN Hongyun, BA Yinggui. Antagonistic Effect of Salidroside on Podocyte Pyroptosis in Diabetic Kidney Disease Rats under Hypoxia Based on NLRP3/IL-1β/TGF-β1 Pathway [J]. Chinese General Practice, 2024, 27(21): 2617-2622.
[5]	WU Kairui, YE Yu, LI Jiaoyue, PEI Bei, LI Xuejun, CHENG Hongliang. A Multicenter Randomized Controlled Clinical Trial Study on the Effect of Piwei Peiyuan Decoction Combined with Acupuncture in the Treatment of Chronic Atrophic Gastritis with Intestinal Metaplasia [J]. Chinese General Practice, 2024, 27(20): 2466-2475.