Objective To investigate the effects of treatment with nicorandil after Percutaneous Coronary Intervention(PCI)in patients with Acute Coronary Syndrome(ACS)on inflammation-related markers,and to assess its effects on vascular endothelial function.Methods Sixty-six ACS patients who underwent PCI in the Department of Cardiovascular Medicine of the Second Affiliated Hospital of Dalian Medical University from August 2022 to January 2023 were used as the study sample,and were divided into the control group and the experimental group according to the method of completely randomized design,with 33 cases in each group.The control group was treated with conventional therapy,and the experimental group was treated with nicorandil.Inflammatory indexes,homocysteine(Hcy)and adverse reactions in serum were compared between the two groups.Results After nicorandil treatment,the levels of postoperative inflammation-related factors in the control group were higher than that in the experimental group,and the difference was statistically significant(P<0.05);The levels of Hcy after nicorandil treatment were lower than that in the control group,and the difference was statistically significant(P<0.05);and the rate of adverse reactions in the experimental group was higher than that in the control group,and there was no statistical difference(P>0.05).Conclusion Nicorandil application in elderly ACS patients after PCI has a definite efficacy,can optimize the vascular-related inflammatory indexes,reduce homocysteine levels to improve coronary vascular endothelial function,and is suitable for further promotion.

Objective: To explore the mechanism of exosome-derived LncRNA ESCCAL-1 regulating the miR-874 /ITGBL1 axis in the progression of colorectal cancer ( CRC) ． Methods : The differentially expressed genes in CRC were analyzed using the Gene Expression Omnibus( GEO) database．Expressions of LncRNA ESCCAL-1，miR-874 and ITGBL1 in CRC tissues and cell lines (SW480，SW620，HCT116 and HT29) and adjacent normal tissues and NCM460 cell lines were detected by qRT-PCR ; 3-( 4，5-dimethylthiazol-2-yl ) -2，5diphenyltetrazoliumbromide (MTT) ，clone formation and flow cytometry was used to detect cell proliferation，colony formation and apoptosis ; dual luciferase reporter assays were used to verify the interaction between miR-874 and ESCCAL-1，ITGBL1 ; fluorescence in situ hybridization was used to determine the subcellular localization of LncRNAESCCAL-1 ．Exosomes were isolated from serum using the Exosome extraction kit. Results : The expressions of ESCCAL-1 and ITGBL1 in CRC tissues and cell lines were higher than those in adjacent normal tissues and NCM460 cell lines，while the opposite was true for miR-874 (P＜0. 05) ．Knockdown of ESCCAL-1 can inhibit CRC cell proliferation and colony formation and promote apoptosis．There are specific binding sites formiR-874 and ESCCAL-1，and miR-874 inhibitor could partially reverse the effect of knockdown ESCCAL-1 in CRC (P＜0. 05) ．ESCCAL-1 upregulates ITGBL1 by adsorbing miR-874．The serum levels of ESCCAL-1 and exo-ESCCAL-1 in CRC patients were higher than those in the control group．Serum exo-ESCCAL-1 may be a valuable diagnostic indicator for CRC treatment (P＜0. 05) . Conclusion ESCCAL-1 promotes CRC progression by regulating the miR-874/ ITGBL1 axis，and ESCCAL-1 may be an effective molecular target for CRC therapy.