Objective:To explore the clinicopathological features of serum alpha-fetoprotein-producing gastric cancer (AFPGC) and its subtype hepatoid adenocarcinoma of the stomach (HAS), and to analyze the related factors affecting the prognosis of AFPGC and HAS patients.Methods:The clinical data of 91 patients with AFPGC who were admitted to the Second Affiliated Hospital of Dalian Medical University from February, 2010 to February, 2021 were retrospectively collected. According to the results of hepatoid differentiation, the patients were divided into HAS group (26 cases) and non-HAS group (65 cases). Meanwhile, 130 patients with alpha-fetoprotein (AFP) negative gastric cancer at the Second Affiliated Hospital of Dalian Medical University were selected by stratified sampling method as common gastric cancer group. The clinicopathological data of patients in the HAS group, non-HAS group and common gastric cancer group were compared and all the patients were followed up for 3 years. Kaplan-Meier survival curves were plotted, and log-rank test was used to analyze the median survival time. Multivariate Cox regression was performed to analyze the independent risk factors affecting the prognosis of patients. Chi-square test was used for statistical comparison.Results:The proportion of patients with poorly differentiated tumor in the HAS group was higher than that in the non-HAS group (84.6%(22/26) vs. 55.4%(36/65)), and the difference was statistically significant ( χ2=7.02, P=0.030). The proportions of patients with age < 60 years old, abnormal level of carcinoembryonic antigen (CEA), vascular tumor thrombus, liver metastasis, poor differentiated tumor, and postoperative chemotherapy in the HAS group were higher than those in the common gastric cancer group (34.6% (9/26) vs. 13.8% (18/130), 26.9% (7/26) vs. 7.7% (10/130), 73.1% (19/26) vs. 51.5% (67/130), 30.8% (8/26) vs. 11.5% (15/130), 84.6% (22/26) vs. 37.7% (49/130), and 69.2% (18/26) vs. 27.7% (36/130), respectively), and the differences were all statistically significant ( χ2=5.16, 6.39, 4.06, 4.94, 18.73, and 16.52; all P<0.05). The proportion of male patients in the non-HAS group was lower than that in the common gastric cancer group (58.5%(38/65) vs. 73.1%(95/130)), while the proportions of patients with age < 60 years old, abnormal levels of carbohydrate antigen (CA)15-3, CA19-9, CA242, and CEA in the non-HAS group were higher than those in the common gastric cancer group (40.0% (26/65) vs. 13.8%(18/130), 7.7%(5/65) vs. 0, 23.1%(15/65) vs. 10.0%(13/130), 18.5%(12/65) vs. 7.7%(10/130), and 23.1%(15/65) vs. 7.7%(10/130), respectively), and the differences were all statistically significant ( χ2=4.27, 16.69, 11.25, 6.03, 5.02, and 9.18; all P<0.05). The proportion of patients with maximum diameter of tumor ≥ 5 cm, clinical stage Ⅲ or Ⅳ, lymph node metastasis, extrahepatic metastasis, and postoperative chemotherapy in the non-HAS group were all higher than those in the common gastric cancer group (58.5% (38/65) vs. 42.3% (55/130), 64.6% (42/65) vs. 46.2% (60/130), 83.1% (54/65) vs. 54.6% (71/130), 47.7% (31/65) vs. 15.4% (20/130), and 75.4% (49/65) vs. 27.7% (36/130), respectively), and the differences were all statistically significant ( χ2=4.53, 10.80, 15.26, 23.41, and 40.08; all P<0.05). The incidence of liver metastasis in patients with AFP >100 μg/L was higher than that in patients with AFP ≤100 μg/L (47.6%(10/21) vs. 17.1%(12/70)), and the difference was statistically significant ( χ2=8.18, P=0.004). The results of Kaplan-Meier survival analysis showed that the median survival time of patients in the HAS group, non-HAS group and common gastric cancer group was 13, 28, and 54 months, respectively, and the difference was statistically significant (log-rank test, χ2=20.33, P<0.001). The results of multivariate Cox regression analysis revealed that CA19-9 ( HR=5.803, 95% confidence interval (95% CI): 1.545 to 21.794, P<0.001) and extrahepatic metastasis ( HR=2.747, 95% CI: 1.243 to 6.068, P=0.012) were independent risk factors affecting the prognosis of patients in the non-HAS group. CA15-3 ( HR=84.163, 95% CI: 5.085 to 1 392.920, P=0.002), CA125 ( HR=0.038, 95% CI: 0.006 to 0.257, P=0.001), and the degree of tumor differentiation ( HR=2.284, 95% CI: 1.101 to 36.677, P=0.039) were independent risk factors affecting the prognosis of patients in the HAS group. Conclusions:Compared to common gastric cancer, AFPGC is characterized by advanced clinical stages, with higher propensity for lymph node metastasis, liver metastasis, extrahepatic metastasis and poor prognosis. The higher the AFP level before surgery, the more possibility of liver metastasis after surgery. Serum CA15-3 and CA125 might be tumor markers in predicting the prognosis of HAS patients.

Aim To investigate the mechanism of in-testinal mucosal barrier protective effect of Qingjie Huagong decoction(QJHGD)on rats with severe acute pancreatitis(SAP).Methods The SAP rat model was constructed,and the sham-operation group,the model group,the group administered with different dosages of QJHGD,and the positive control group were set up respectively.HE staining was used to observe the histopathological changes.ELISA was employed to detect the serum levels of diamine oxidase(DAO)and D-lactic acid(D-LA)in rats.Transmission electron microscopy was utilized to observe the mitochondria of ileal tissues.qRT-PCR and Western blot were applied to detect the mRNA and protein expression of PGAM5,Drp1,PINK1,Parkin,LC3B in ileal tissues of rats.Results Compared with the sham-operated group,the pancreas and ileum tissues of rats in the model group showed obvious pathological changes,with abnormal mitochondrial structure and reduced number of autoph-agic vesicles in the ileum tissues.The levels of DAO and D-LA in serum increased(P＜0.01),and the mRNA and protein expression of PGAM 5,Drp 1,PINK1,Parkin,and LC3B in the ileum tissues de-creased significantly.Compared with the model group,pancreatic and ileal pathology were improved,mito-chondrial damage in the ileum was reduced,and the number of autophagic vesicles increased in the QJHGD group.The serum levels of DAO and D-LA were re-duced,and the expression of PGAM5,Drp1,PINK1,Parkin,and LC3B mRNA and protein in the ileal tis-sues increased significantly.Conclusions QJHGD may exert a protective effect on the SAP intestinal mu-cosal barrier by regulating the PGAM5/Drp1/PINK1/Parkin axis in order to elevate the level of mitochondri-al autophagy in the intestinal epithelial cells,thereby improving the level of repair of the intestinal epithelial cells.

The study aimed to investigate the effect of the CD200R1 gene deletion on microglia activation and nigrostriatal dopamine neuron loss in the Parkinson's disease (PD) process. The CRISPR-Cas9 technology was applied to construct the CD200R1^-/- mice. The primary microglia cells of wild-type and CD200R1^-/- mice were cultured and treated with bacterial lipopolysaccharide (LPS). Microglia phagocytosis level was assessed by a fluorescent microsphere phagocytosis assay. PD mouse model was prepared by nigral stereotaxic injection of recombinant adeno-associated virus vector carrying human α-synuclein (α-syn). The changes in the motor behavior of the mice with both genotypes were evaluated by cylinder test, open field test, and rotarod test. Immunohistochemical staining was used to assess the loss of dopamine neurons in substantia nigra. Immunofluorescence staining was used to detect the expression level of CD68 (a key molecule involved in phagocytosis) in microglia. The results showed that CD200R1 deletion markedly enhanced LPS-induced phagocytosis in vitro by the microglial cells. In the mouse model of PD, CD200R1 deletion exacerbated motor behavior impairment and dopamine neuron loss in substantia nigra. Fluorescence intensity analysis results revealed a significant increase in CD68 expression in microglia located in the substantia nigra of CD200R1^-/- mice. The above results suggest that CD200R1 deletion may further activates microglia by promoting microglial phagocytosis, leading to increased loss of the nigrostriatal dopamine neurons in the PD model mice. Therefore, targeting CD200R1 could potentially serve as a novel therapeutic target for the treatment of early-stage PD.
Animals ; Microglia/physiology* ; Mice ; Phagocytosis ; Parkinson Disease/genetics* ; Disease Models, Animal ; Receptors, Cell Surface/physiology* ; Dopaminergic Neurons/pathology* ; Antigens, CD/metabolism* ; Gene Deletion ; Substantia Nigra ; Mice, Inbred C57BL ; Mice, Knockout ; Cells, Cultured ; Male ; alpha-Synuclein ; CD68 Molecule ; Orexin Receptors

OBJECTIVE: Peritoneal fibrosis (PF) is an adverse event that occurs during long-term peritoneal dialysis, significantly impairing treatment efficiency and adversely affecting patient outcomes. Astragaloside IV (AS-IV), a principal active component derived from Astragalus membranaceus (Fisch.) Bunge, has exhibited anti-inflammatory and antifibrotic effects in various settings. This study aims to investigate the potential therapeutic efficacy and mechanism of AS-IV in the treatment of PF. METHODS: The PF mouse model was established by intraperitoneal injection of 4.25% peritoneal dialysis fluid (100 mL/kg). The epithelial-mesenchymal transition (EMT) of HMrSV5 cells was induced by the addition of 10 ng/mL transforming growth factor β (TGF-β). The differentially expressed genes in HMrSV5 cells treated with AS-IV were screened using transcriptome sequencing analysis. The potential targets of AS-IV were screened using network pharmacology and analyzed using molecular docking and molecular dynamics simulations. RESULTS: Administration of AS-IV at doses of 20, 40, or 80 mg/kg effectively mitigated the increase in peritoneal thickness and the development of fibrosis in mice with PF. The expression of the fibrosis marker α-smooth muscle actin in the peritoneum was significantly decreased in AS-IV-treated mice. The treatment of AS-IV (10, 20, and 40 μmol/L) significantly delayed the EMT of HMrSV5 cells induced by TGF-β, as demonstrated by the decreased number of 5-ethynyl-2'-deoxyuridine-positive cells, reduced migrated area, and decreased expression of fibrosis markers. A total of 460 differentially expressed genes were detected in AS-IV-treated HMrSV5 cells through transcriptome sequencing, with notable enrichment in the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)-AKT serine/threonine kinase 1 (AKT) signaling pathway. The reduced levels of phosphorylated PI3K (p-PI3K) and p-AKT were detected in HMrSV5 cells with AS-IV treatment. Epidermal growth factor receptor (EGFR) was predicted as a direct target of AS-IV, exhibiting strong hydrogen bond interactions. The activation of the PI3K-AKT pathway by the compound 740Y-P, and the activation of the EGFR pathway by NSC 228155 each partially counteracted the inhibitory effect of AS-IV on the EMT of HMrSV5 cells. CONCLUSION AS-IV delayed the EMT process in peritoneal mesothelial cells and slowed the progression of PF, potentially serving as a therapeutic agent for the early prevention and treatment of PF. Please cite this article as: Huang Y, Chu CL, Qiu WH, Chen JY, Cao LX, Ji SY, Zhu B, Wang GK, Shen QQ. Astragaloside IV delayed the epithelial-mesenchymal transition in peritoneal fibrosis by inhibiting the activation of EGFR and PI3K-AKT pathways. J Integr Med. 2025; 23(6):694-705.
Epithelial-Mesenchymal Transition/drug effects* ; Animals ; Saponins/pharmacology* ; Triterpenes/pharmacology* ; Mice ; Peritoneal Fibrosis/pathology* ; Proto-Oncogene Proteins c-akt/metabolism* ; ErbB Receptors/metabolism* ; Phosphatidylinositol 3-Kinases/metabolism* ; Signal Transduction/drug effects* ; Male ; Humans ; Molecular Docking Simulation ; Cell Line ; Mice, Inbred C57BL

Aim To explore the therapeutic effect and mechanism of Qingjie Huagong decoction in modulating PI3K/AKT/NF-κB signaling pathway in inflammatory response of acute pancreatitis(AP)mice.Methods Twenty-four mice were randomly divided into Blank group,Model group,Ustekin group,and Qingjie Hua-gong decoction group,with six mice in each group.The AP model was prepared by using rain frogin.Serum α-AMS,PNLP,IL-1β,IL-6,IL-8,IL-18,and TNF-α lev-els were detected by ELISA;the pancreatic pathology was detected by HE staining;the expressions of PI3K,AKT,and NF-κB-related proteins and mRNAs were de-tected by immunohistochemistry,Western blot,and RT-qPCR.Results Compared with the blank group,the model group showed obvious pathological damage to the pancreas,with significantly higher serum α-AMS,PN-LP,IL-1β,IL-6,IL-8,IL-18,and TNF-α levels(P＜0.01),and significantly higher levels of PI3K,AKT,and NF-κB-related proteins and mRNA expression(P＜0.01).Compared with the model group,both the Qingjie Huagong decoction group and the ustekin group improved the histopathological changes in the pancreas of AP mice,decreased the serum α-AMS,PNLP,IL-1β,IL-6,IL-8,IL-18,and TNF-α levels,and down-reg-ulated the expression levels of pancreatic PI3K,AKT,NF-κB-related proteins and mRNA(P＜0.05 or P＜0.01).Conclusion Qingjie Huagong decoction may inhibit the inflammatory response and protect pancreat-ic tissues by regulating the expression of PI3K/AKT/NF-κB signaling pathway.

Aim To explore the therapeutic effect and mechanism of Qingjie Huagong decoction in modulating PI3K/AKT/NF-κB signaling pathway in inflammatory response of acute pancreatitis(AP)mice.Methods Twenty-four mice were randomly divided into Blank group,Model group,Ustekin group,and Qingjie Hua-gong decoction group,with six mice in each group.The AP model was prepared by using rain frogin.Serum α-AMS,PNLP,IL-1β,IL-6,IL-8,IL-18,and TNF-α lev-els were detected by ELISA;the pancreatic pathology was detected by HE staining;the expressions of PI3K,AKT,and NF-κB-related proteins and mRNAs were de-tected by immunohistochemistry,Western blot,and RT-qPCR.Results Compared with the blank group,the model group showed obvious pathological damage to the pancreas,with significantly higher serum α-AMS,PN-LP,IL-1β,IL-6,IL-8,IL-18,and TNF-α levels(P＜0.01),and significantly higher levels of PI3K,AKT,and NF-κB-related proteins and mRNA expression(P＜0.01).Compared with the model group,both the Qingjie Huagong decoction group and the ustekin group improved the histopathological changes in the pancreas of AP mice,decreased the serum α-AMS,PNLP,IL-1β,IL-6,IL-8,IL-18,and TNF-α levels,and down-reg-ulated the expression levels of pancreatic PI3K,AKT,NF-κB-related proteins and mRNA(P＜0.05 or P＜0.01).Conclusion Qingjie Huagong decoction may inhibit the inflammatory response and protect pancreat-ic tissues by regulating the expression of PI3K/AKT/NF-κB signaling pathway.

Aim To investigate the mechanism of in-testinal mucosal barrier protective effect of Qingjie Huagong decoction(QJHGD)on rats with severe acute pancreatitis(SAP).Methods The SAP rat model was constructed,and the sham-operation group,the model group,the group administered with different dosages of QJHGD,and the positive control group were set up respectively.HE staining was used to observe the histopathological changes.ELISA was employed to detect the serum levels of diamine oxidase(DAO)and D-lactic acid(D-LA)in rats.Transmission electron microscopy was utilized to observe the mitochondria of ileal tissues.qRT-PCR and Western blot were applied to detect the mRNA and protein expression of PGAM5,Drp1,PINK1,Parkin,LC3B in ileal tissues of rats.Results Compared with the sham-operated group,the pancreas and ileum tissues of rats in the model group showed obvious pathological changes,with abnormal mitochondrial structure and reduced number of autoph-agic vesicles in the ileum tissues.The levels of DAO and D-LA in serum increased(P＜0.01),and the mRNA and protein expression of PGAM 5,Drp 1,PINK1,Parkin,and LC3B in the ileum tissues de-creased significantly.Compared with the model group,pancreatic and ileal pathology were improved,mito-chondrial damage in the ileum was reduced,and the number of autophagic vesicles increased in the QJHGD group.The serum levels of DAO and D-LA were re-duced,and the expression of PGAM5,Drp1,PINK1,Parkin,and LC3B mRNA and protein in the ileal tis-sues increased significantly.Conclusions QJHGD may exert a protective effect on the SAP intestinal mu-cosal barrier by regulating the PGAM5/Drp1/PINK1/Parkin axis in order to elevate the level of mitochondri-al autophagy in the intestinal epithelial cells,thereby improving the level of repair of the intestinal epithelial cells.

Objective:To explore the clinicopathological features of serum alpha-fetoprotein-producing gastric cancer (AFPGC) and its subtype hepatoid adenocarcinoma of the stomach (HAS), and to analyze the related factors affecting the prognosis of AFPGC and HAS patients.Methods:The clinical data of 91 patients with AFPGC who were admitted to the Second Affiliated Hospital of Dalian Medical University from February, 2010 to February, 2021 were retrospectively collected. According to the results of hepatoid differentiation, the patients were divided into HAS group (26 cases) and non-HAS group (65 cases). Meanwhile, 130 patients with alpha-fetoprotein (AFP) negative gastric cancer at the Second Affiliated Hospital of Dalian Medical University were selected by stratified sampling method as common gastric cancer group. The clinicopathological data of patients in the HAS group, non-HAS group and common gastric cancer group were compared and all the patients were followed up for 3 years. Kaplan-Meier survival curves were plotted, and log-rank test was used to analyze the median survival time. Multivariate Cox regression was performed to analyze the independent risk factors affecting the prognosis of patients. Chi-square test was used for statistical comparison.Results:The proportion of patients with poorly differentiated tumor in the HAS group was higher than that in the non-HAS group (84.6%(22/26) vs. 55.4%(36/65)), and the difference was statistically significant ( χ2=7.02, P=0.030). The proportions of patients with age < 60 years old, abnormal level of carcinoembryonic antigen (CEA), vascular tumor thrombus, liver metastasis, poor differentiated tumor, and postoperative chemotherapy in the HAS group were higher than those in the common gastric cancer group (34.6% (9/26) vs. 13.8% (18/130), 26.9% (7/26) vs. 7.7% (10/130), 73.1% (19/26) vs. 51.5% (67/130), 30.8% (8/26) vs. 11.5% (15/130), 84.6% (22/26) vs. 37.7% (49/130), and 69.2% (18/26) vs. 27.7% (36/130), respectively), and the differences were all statistically significant ( χ2=5.16, 6.39, 4.06, 4.94, 18.73, and 16.52; all P<0.05). The proportion of male patients in the non-HAS group was lower than that in the common gastric cancer group (58.5%(38/65) vs. 73.1%(95/130)), while the proportions of patients with age < 60 years old, abnormal levels of carbohydrate antigen (CA)15-3, CA19-9, CA242, and CEA in the non-HAS group were higher than those in the common gastric cancer group (40.0% (26/65) vs. 13.8%(18/130), 7.7%(5/65) vs. 0, 23.1%(15/65) vs. 10.0%(13/130), 18.5%(12/65) vs. 7.7%(10/130), and 23.1%(15/65) vs. 7.7%(10/130), respectively), and the differences were all statistically significant ( χ2=4.27, 16.69, 11.25, 6.03, 5.02, and 9.18; all P<0.05). The proportion of patients with maximum diameter of tumor ≥ 5 cm, clinical stage Ⅲ or Ⅳ, lymph node metastasis, extrahepatic metastasis, and postoperative chemotherapy in the non-HAS group were all higher than those in the common gastric cancer group (58.5% (38/65) vs. 42.3% (55/130), 64.6% (42/65) vs. 46.2% (60/130), 83.1% (54/65) vs. 54.6% (71/130), 47.7% (31/65) vs. 15.4% (20/130), and 75.4% (49/65) vs. 27.7% (36/130), respectively), and the differences were all statistically significant ( χ2=4.53, 10.80, 15.26, 23.41, and 40.08; all P<0.05). The incidence of liver metastasis in patients with AFP >100 μg/L was higher than that in patients with AFP ≤100 μg/L (47.6%(10/21) vs. 17.1%(12/70)), and the difference was statistically significant ( χ2=8.18, P=0.004). The results of Kaplan-Meier survival analysis showed that the median survival time of patients in the HAS group, non-HAS group and common gastric cancer group was 13, 28, and 54 months, respectively, and the difference was statistically significant (log-rank test, χ2=20.33, P<0.001). The results of multivariate Cox regression analysis revealed that CA19-9 ( HR=5.803, 95% confidence interval (95% CI): 1.545 to 21.794, P<0.001) and extrahepatic metastasis ( HR=2.747, 95% CI: 1.243 to 6.068, P=0.012) were independent risk factors affecting the prognosis of patients in the non-HAS group. CA15-3 ( HR=84.163, 95% CI: 5.085 to 1 392.920, P=0.002), CA125 ( HR=0.038, 95% CI: 0.006 to 0.257, P=0.001), and the degree of tumor differentiation ( HR=2.284, 95% CI: 1.101 to 36.677, P=0.039) were independent risk factors affecting the prognosis of patients in the HAS group. Conclusions:Compared to common gastric cancer, AFPGC is characterized by advanced clinical stages, with higher propensity for lymph node metastasis, liver metastasis, extrahepatic metastasis and poor prognosis. The higher the AFP level before surgery, the more possibility of liver metastasis after surgery. Serum CA15-3 and CA125 might be tumor markers in predicting the prognosis of HAS patients.

Objective To investigate the incidence rate,clinical characteristics,and prognosis of neonatal stroke in Shenzhen,China.Methods Led by Shenzhen Children's Hospital,the Shenzhen Neonatal Data Collaboration Network organized 21 institutions to collect 36 cases of neonatal stroke from January 2020 to December 2022.The incidence,clinical characteristics,treatment,and prognosis of neonatal stroke in Shenzhen were analyzed.Results The incidence rate of neonatal stroke in 21 hospitals from 2020 to 2022 was 1/15 137,1/6 060,and 1/7 704,respectively.Ischemic stroke accounted for 75％(27/36);boys accounted for 64％(23/36).Among the 36 neonates,31(86％)had disease onset within 3 days after birth,and 19(53％)had convulsion as the initial presentation.Cerebral MRI showed that 22 neonates(61％)had left cerebral infarction and 13(36％)had basal ganglia infarction.Magnetic resonance angiography was performed for 12 neonates,among whom 9(75％)had involvement of the middle cerebral artery.Electroencephalography was performed for 29 neonates,with sharp waves in 21 neonates(72％)and seizures in 10 neonates(34％).Symptomatic/supportive treatment varied across different hospitals.Neonatal Behavioral Neurological Assessment was performed for 12 neonates(33％,12/36),with a mean score of(32±4)points.The prognosis of 27 neonates was followed up to around 12 months of age,with 44％(12/27)of the neonates having a good prognosis.Conclusions Ischemic stroke is the main type of neonatal stroke,often with convulsions as the initial presentation,involvement of the middle cerebral artery,sharp waves on electroencephalography,and a relatively low neurodevelopment score.Symptomatic/supportive treatment is the main treatment method,and some neonates tend to have a poor prognosis.

Aim To explore the therapeutic effect of Qingjie Huagong decoction in regulating RIPK1/RIPK3/MLKL signaling pathway on pancreatic necrotic apoptosis in rats with severe acute pancreatitis(SAP)and the underlying mechanism.Methods The SAP rat model was established by retrograde pancreaticobili-ary injection of sodium taurocholate,and the sham-op-eration group,the model group,the group with differ-ent dosages of Qingjie Huagong decoction and the posi-tive control group were set up respectively.The group with different dosages of Qingjie Huagong decoction was given low,medium and high dosages of traditional Chinese medicine in the gastric gavage,the positive control group was given ulinastatin drug intervention,and the sham-operation and the model group were giv-en physiological saline in the gastric gavage;HE stai-ning was applied to observe pancreatic pathology;ELISA was used to measure the serum levels of α-am-ylase,IL-1β,IL-6,and TNF-α;immunohistochemis-try and Western blot were employed to determine the RIPK1,RIPK3,MLKL protein expression in rat pan-creatic tissue;and qRT-PCR was utilized to detect the transcription levels of R1PK1,RIPK3 and MLKL mR-NA in rat pancreatic tissue.Results Compared with the sham-operated group,the model group showed dif-fuse necrosis of pancreatic acinar cells,obvious inter-lobular septal edema,inflammatory cell infiltration,significantly higher levels of α-amylase,IL-1β,IL-6,and TNF-α(P＜0.01),and significantly higher ex-pression levels of RIPK1,RIPK3,and MLKL proteins and mRNAs(P＜0.01)in the model group;com-pared with the model group,the Qingjie Huagong de-coction dose groups and positive control group signifi-cantly improved pancreatic histopathology,reduced pancreatic tissue necrosis and apoptosis,lowered the expression levels of α-amylase,IL-1 β,IL-6 and TNF-α(P＜0.01),and reduced the expression levels of RIPK1,RIPK3,and MLKL proteins and mRNAs(P＜0.01).Conclusions Qingjie Huagong decoction may improve the necrotic apoptosis of pancreatic tissue by regulating the RIPK1/RIPK3/MLKL signaling path-way,thus playing a role in protecting pancreatic tissue and slowing down the progression of the disease.