ObjectiveTo explore the effect of semaglutide （SEM） on myocardial injury induced by coronary microembolization （CME） in rats via the adenosine monophosphate-activated protein kinase （AMPK）/nucleotide-binding oligomerization domain-like receptor protein 3 （NLRP3） signaling pathway. MethodsThirty-two rats were randomly assigned to four groups （n=8）： the Sham group， the CME group， the CME + SEM group， and the CME + SEM + Compound C （CC， a specific inhibitor of AMPK） group. The CME model was established by injecting microembolic spheres into the left ventricle， while the Sham group received an equal volume of normal saline via left ventricular injection. The CME + SEM group received subcutaneous injections of SEM （1 mg/kg， once weekly） for 4 weeks before CME induction. For the CME + SEM + CC group， rats were treated with SEM for 4 weeks， followed by an intravenous injection of CC （0.25 mg/kg dissolved in sterile normal saline） 30 minutes before CME modeling. 24 hours post-modeling， all groups underwent the following assessments： echocardiography to evaluate cardiac function， HE staining for myocardial histopathological analysis， Heidenhain staining to quantify the microinfarct area， ELISA to determine serum cardiac troponin T （cTnT） levels， and Western blot analysis to detect the expression of proteins related to the AMPK/NLRP3 pathway in cardiac tissues. ResultsCompared with the Sham group， the CME group showed significantly deteriorated cardiac function， elevated serum cTnT levels， and a marked increase in myocardial microinfarct area （P<0.05）. Compared with the CME group， the CME + SEM group exhibited significant improvements in cardiac function， decreased cTnT levels， and a remarkable reduction in myocardial microinfarct area （P<0.05）. Histopathological analysis revealed a normal myocardial structure in the Sham group without infarction. In contrast， the CME group showed disorganized myocardial arrangement， accompanied by nuclear fragmentation and karyolysis. In the CME + SEM group， myocardial degeneration， edema and inflammatory cell infiltration were obviously alleviated. Compared with Sham group， the protein ratio of p-AMPK/AMPK slightly increased in the CME group， while the protein levels of NLRP3， gasdermin D-N domain （GSDMD-N）， apoptosis-associated speck-like protein containing a CARD （ASC）， caspase-1 p20， interleukin（IL）-1β ， and IL-18 were markedly upregulated （P<0.05）. Notably， compared to the CME group， the CME + SEM group had a further elevated p-AMPK/AMPK ratio， while the protein levels of NLRP3， GSDMD-N， ASC， caspase-1 p20， IL-1β and IL-18 were markedly decreased （P<0.05）. ConclusionSEM significantly ameliorates CME-induced myocardial injury， and its mechanism of action may be closely associated with promoting AMPK phosphorylation， inhibiting NLRP3 inflammasome-mediated inflammatory responses， and suppressing pyroptosis.

Objective:To evaluate the clinical value of sacral canal posterior wall reconstruction in the treatment of symptomatic sacral canal cysts.Methods:A retrospective cohort study was conducted.The clinical data of 80 patients with symptomatic sacral cysts who underwent surgical treatment at Beijing Friendship Hospital, Capital Medical University, between June 2018 and September 2024 were collected. There were 19 males and 61 females, with an average age of (49.0±11.3) years (ranged from 23-76 years). The patients were divided into the traditional group ( n=30) and the reconstruction group ( n=50) based on the surgical approach. The traditional group underwent the conventional surgical method without reconstruction of the posterior wall of the sacral canal, while the reconstruction group underwent posterior wall reconstruction of the sacral canal. Postoperative observations included the integrity of the sacral canal posterior wall, wound healing, and symptom improvement in both groups. Measurement data with normal distribution were expressed as mean±standard deviation( ± s). Independent samples t-test was used for comparisons of measurement data between groups. Categorical data were compared using the chi-square test or Fisher′s exact test. Ordinal data were analyzed using the Mann-Whitney U test. Pearson correlation analysis was used to assess the relationship between variables. Results:Among the 80 patients, the sacral bone integrity score in the reconstruction group was (1.42±0.49) scores, compared to (3.00±0.00) scores in the traditional group, the reconstruction group showed significantly better results ( P<0.05). Symptom improvement was also significantly different between the two groups ( P=0.038): in the traditional group, 17 patients experienced complete symptom resolution, 6 partial improvement, 7 no improvement, and 0 worsening; in the reconstruction group, 37 had complete symptom resolution, 11 partial improvement, 2 no improvement, and 0 worsening. The effective improvement rate (complete+ partial improvement) in the reconstruction group was significantly better than that in the traditional group ( P=0.012). In terms of wound healing, 76 cases healed well, 4 had delayed healing, and 0 had infections. In the traditional group, 27 healed well, 3 had delayed healing, 0 infections; in the reconstruction group, 49 healed well, 1 had delayed healing, and 0 infections. There was no significant difference in wound healing rate between the two groups ( P=0.146). A significant positive correlation was found between sacral canal posterior wall integrity and symptom improvement ( r=0.288, P=0.010). Conclusion:Sacral canal posterior wall reconstruction significantly improves postoperative anatomical integrity and clinical outcomes without increasing complications, supporting its adoption as a preferred surgical approach for symptomatic sacral canal cysts.

AIM:To investigate the protective effect of Shexiang-Tongxin dropping pills(STDP)against myo-cardial injury induced by coronary microembolization(CME)in rats,with a focus on the cyclic GMP-AMP synthase(cGAS)-stimulator of interferon genes(STING)signaling pathway.METHODS:Thirty-two Sprague-Dawley rats were randomly allocated into four groups using a random number table:sham group,CME group,STDP group,and RU.521 group,with 8 rats per group.A rat model of CME was established via the injection of embolic microspheres into the left ventricle.The rats in sham group received an equal volume of normal saline via left ventricular injection instead,those in STDP group were given STDP(40 mg/kg)by oral gavage once daily for 14 consecutive days before CME modeling,and those in RU.521 group were intraperitoneally injected with RU.521(5 mg/kg)once daily for 7 consecutive days before CME modeling.Echocardiography was performed to evaluate cardiac function 24 h after modeling.HE staining was used to observe pathological changes in myocardial tissue,and TTC staining was applied to detect myocardial infarction areas.Enzyme-linked immunosorbent assay(ELISA)was used to measure levels of interleukin(IL)-1β and tumor necrosis factor(TNF)-α.A commercial assay kit was employed to detect myocardial injury marker cardiac troponin I(cTnI).Western blot was performed to analyze the expression of cGAS-STING pathway-related proteins in cardiac tissues.RESULTS:Compared with sham group,the rats in CME group exhibited significantly impaired cardiac function and a marked increase in serum cTnI levels(P<0.05).In contrast,compared with CME group,the rats in both STDP group and RU.521 group demonstrated significant improvements in cardiac function and reductions in cTnI levels((P<0.05).Furthermore,HE staining and TTC staining revealed that the rats in CME group had loosely arranged myocardial fibers,swollen cardiomyo-cytes,and an increased myocardial infarction erea compared with sham group(P<0.05).Meanwhile,the expression lev-els of inflammatory factors IL-1β and TNF-α,as well as the relative expression of cGAS,STING and NF-κB p-p65 pro-teins were significantly increased(P<0.05).In comparison,the rats in STDP group and RU.521 group showed a signifi-cant reduction in myocardial infarction area,down-regulated expression of cGAS,STING,and NF-κB p-p65 proteins,and markedly decreased levels of IL-1β and TNF-α compared with CME group(P<0.05).CONCLUSION:STDP pre-treatment ameliorated myocardial injury,cardiac dysfunction and myocardial infarct size induced by CME.The underlying mechenism may involve the suppression of the cGAS-STING signaling pathway,thereby attenuating myocardial inflamma-tion after CME.

AIM:To investigate the protective effect of Shexiang-Tongxin dropping pills(STDP)against myo-cardial injury induced by coronary microembolization(CME)in rats,with a focus on the cyclic GMP-AMP synthase(cGAS)-stimulator of interferon genes(STING)signaling pathway.METHODS:Thirty-two Sprague-Dawley rats were randomly allocated into four groups using a random number table:sham group,CME group,STDP group,and RU.521 group,with 8 rats per group.A rat model of CME was established via the injection of embolic microspheres into the left ventricle.The rats in sham group received an equal volume of normal saline via left ventricular injection instead,those in STDP group were given STDP(40 mg/kg)by oral gavage once daily for 14 consecutive days before CME modeling,and those in RU.521 group were intraperitoneally injected with RU.521(5 mg/kg)once daily for 7 consecutive days before CME modeling.Echocardiography was performed to evaluate cardiac function 24 h after modeling.HE staining was used to observe pathological changes in myocardial tissue,and TTC staining was applied to detect myocardial infarction areas.Enzyme-linked immunosorbent assay(ELISA)was used to measure levels of interleukin(IL)-1β and tumor necrosis factor(TNF)-α.A commercial assay kit was employed to detect myocardial injury marker cardiac troponin I(cTnI).Western blot was performed to analyze the expression of cGAS-STING pathway-related proteins in cardiac tissues.RESULTS:Compared with sham group,the rats in CME group exhibited significantly impaired cardiac function and a marked increase in serum cTnI levels(P<0.05).In contrast,compared with CME group,the rats in both STDP group and RU.521 group demonstrated significant improvements in cardiac function and reductions in cTnI levels((P<0.05).Furthermore,HE staining and TTC staining revealed that the rats in CME group had loosely arranged myocardial fibers,swollen cardiomyo-cytes,and an increased myocardial infarction erea compared with sham group(P<0.05).Meanwhile,the expression lev-els of inflammatory factors IL-1β and TNF-α,as well as the relative expression of cGAS,STING and NF-κB p-p65 pro-teins were significantly increased(P<0.05).In comparison,the rats in STDP group and RU.521 group showed a signifi-cant reduction in myocardial infarction area,down-regulated expression of cGAS,STING,and NF-κB p-p65 proteins,and markedly decreased levels of IL-1β and TNF-α compared with CME group(P<0.05).CONCLUSION:STDP pre-treatment ameliorated myocardial injury,cardiac dysfunction and myocardial infarct size induced by CME.The underlying mechenism may involve the suppression of the cGAS-STING signaling pathway,thereby attenuating myocardial inflamma-tion after CME.

Angioplasty, Balloon, Coronary ; Heart Injuries ; drug therapy ; etiology ; Humans ; Thrombin ; administration & dosage

0. 05). In glioma, the expression level was higher in glioblastornathan in oligodendroglial tumors (P = 0. 011). While the frequency of promoter methylation of RASSFof RASSF1A gene was 39. 3% . It was not found the promoter methylation in normal brain tissues and U251 cell line. In 11 patients with the aberrant promoter methylation, five showed the gene inactivation (P = 0. 022). Conclusion Aberrant promoter methylation was found in glioma. Although the gene inactivation of RASSF1 A was not so common in glioma, its expression was lower in glioma than in normal brain tissues. Promoter methylation may contribute to the low level or loss of RASSFT A mRNA expression.