Acute pancreatitis(AP)is a common and severe digestive disease in dogs,characterized by a high recurrence rate and complications that significantly impact canine health.This study in-vestigates the mechanism by which adipose-derived stem cells(ADSCs)regulate the CHOP/Bcl-2 pathway to mitigate acute pancreatic injury in dogs.Twenty Beagle dogs were randomly divided in-to four groups:a Sham group,an AP model group,an ADSCs treatment group,and a conditioned medium(CM)treatment group.The AP model was established by injecting a mixed solution of trypsin and sodium taurocholate into the AP model group.The ADSCs treatment group received intravenous injections of ADSCs immediately following surgery,while the CM treatment group re-ceived conditioned medium preparations.Pancreatic tissue was collected 24 hours post-surgery,and changes in the CHOP/Bcl-2 pathway were assessed using histopathology,transmission electron microscopy,western blotting,fluorescence quantification,immunofluorescence,and TUNEL stai-ning.The results indicated that AP induced significant interstitial edema,hemorrhage,inflammato-ry cell infiltration,chromatin contraction,and endoplasmic reticulum swelling,the expression lev-els of GRP78 and CHOP were found to be elevated,whereas the expression of Bcl-2 was downreg-ulated.Additionally,the expression levels of BAX,JNK,Caspase-3,and Caspase-12 increased,leading to an increased rate of cell apoptosis.Such changes result in an elevated apoptosis rate and a further decrease in Bcl-2 expression.Both ADSCs and CM therapy were found to alleviate the path-ological damage in pancreatic tissue,resulting in downregulation of CHOP and apoptosis-related markers,upregulation of Bcl-2,and a reduction in the apoptosis rate.The results of this study sug-gest that ADSCs may mitigate acute pancreatic injury induced by trypsin and sodium taurocholate in AP dogs by modulating the CHOP/Bcl-2 pathway.Targeted modulation of the transcriptional activity of CHOP may offer novel therapeutic approaches for AP.

Acute pancreatitis(AP)is a common and severe digestive disease in dogs,characterized by a high recurrence rate and complications that significantly impact canine health.This study in-vestigates the mechanism by which adipose-derived stem cells(ADSCs)regulate the CHOP/Bcl-2 pathway to mitigate acute pancreatic injury in dogs.Twenty Beagle dogs were randomly divided in-to four groups:a Sham group,an AP model group,an ADSCs treatment group,and a conditioned medium(CM)treatment group.The AP model was established by injecting a mixed solution of trypsin and sodium taurocholate into the AP model group.The ADSCs treatment group received intravenous injections of ADSCs immediately following surgery,while the CM treatment group re-ceived conditioned medium preparations.Pancreatic tissue was collected 24 hours post-surgery,and changes in the CHOP/Bcl-2 pathway were assessed using histopathology,transmission electron microscopy,western blotting,fluorescence quantification,immunofluorescence,and TUNEL stai-ning.The results indicated that AP induced significant interstitial edema,hemorrhage,inflammato-ry cell infiltration,chromatin contraction,and endoplasmic reticulum swelling,the expression lev-els of GRP78 and CHOP were found to be elevated,whereas the expression of Bcl-2 was downreg-ulated.Additionally,the expression levels of BAX,JNK,Caspase-3,and Caspase-12 increased,leading to an increased rate of cell apoptosis.Such changes result in an elevated apoptosis rate and a further decrease in Bcl-2 expression.Both ADSCs and CM therapy were found to alleviate the path-ological damage in pancreatic tissue,resulting in downregulation of CHOP and apoptosis-related markers,upregulation of Bcl-2,and a reduction in the apoptosis rate.The results of this study sug-gest that ADSCs may mitigate acute pancreatic injury induced by trypsin and sodium taurocholate in AP dogs by modulating the CHOP/Bcl-2 pathway.Targeted modulation of the transcriptional activity of CHOP may offer novel therapeutic approaches for AP.

Objective To evaluate the protective effect of epigallocatechin-3-gallate(EGCG)on cisplatin(CIS)-induced acute kidney injury(AKI)in rats based on network pharmacology and in vivo animal model experiments.Methods Targets of EGCG and AKI were collected from the TCMSP,Gene Cards,and OMIM websites,and a protein-protein interaction network was constructed based on the intersection.The intersection targets were analyzed visually using Cytoscape 3.9.1 and the key targets were screened out.Kyoto Encyclopedia and of Genes and Genomes and Gene Ontology enrichment analyses were carried out using the DAVID database.Thirty-two male Wistar rats were divided randomly into four groups:CON group,EGCG group,CIS group,and CIS+EGCG group.Rats in the control and CIS groups were given normal saline every day,rats in the EGCG and CIS+EGCG groups were given EGCG(40 mg/kg)every day for 28 d,and rats in the CIS and CIS+EGCG groups received an intraperitoneal injection of CIS(7 mg/kg)on the 26th day.Blood and tissue samples were obtained on the 29th day.Serum urea nitrogen and creatinine levels were detected,renal pathology was observed by HE staining,and apoptosis in renal tissue was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling.Western Blot,qRT-PCR,and immunohistochemistry were used to verify the result.Results Eighty-seven genes intersecting EGCG and AKI and 25 core targets were screened from network pharmacology,which influenced the development of AKI via signal pathways such as PI3K/Akt and various biological processes.EGCG pretreatment significantly reduced serum levels of serum urea nitrogen and creatinine,improved the renal pathology,and reduced renal tissue apoptosis in AKI rats.Western Blot,qRT-PCR and immunohistochemistry showed that pretreatment with EGCG activated the PI3K/Akt pathway.Conclusions EGCG alleviates CIS-induced AKI in rats via the PI3K/Akt signaling pathway.