ObjectiveTo investigate the mechanism of danshenol A （DA） pretreatment in alleviating myocardial ischemia-reperfusion injury （MIRI） by regulating cardiomyocyte ferroptosis by in vivo and in vitro experiments. MethodsA MIRI model was established in SD rats， and an in vitro oxygen-glucose deprivation/reoxygenation （OGD/R） model was constructed with H9C2 cells. Both models were treated with DA. H9C2 cells were allocated into blank， model （OGD/R）， DA， ferroptosis inducer （erastin）， and ferroptosis inhibitor （Fer-1） groups. Cell viability was assessed by the methyl thiazolyl tetrazolium （MTT） assay. Biochemical assays were performed to measure the superoxide dismutase （SOD）， malondialdehyde （MDA）， glutathione （GSH）， and ferrous ion （Fe²⁺） levels. Dihydroethidium （DHE） fluorescence assay was adopted to quantify the reactive oxygen species （ROS） level. Real-time PCR and Western blot were employed to quantify the mRNA and protein levels， respectively， of prostaglandin-endoperoxide synthase 2 （PTGS2）， glutathione peroxidase 4 （GPX4）， ferritin heavy chain 1 （FTH1）， and acyl-coA synthetase long-chain family 4 （ACSL4）. Sixty SPF-grade healthy male SD rats were randomly assigned to control， model （MIRI）， DA， erastin， and Fer-1 groups. Enzyme-linked immunosorbent assay （ELISA） was adopted to measure the serum levels of cardiac troponin I （cTnI）， lactate dehydrogenase （LDH）， and creatine kinase （CK）. Histopathological changes in the myocardial tissue were observed by hematoxylin-eosin （HE） staining. Cardiomyocyte apoptosis was detected by terminal deoxynucleotidyl transferase-mediated nick end labeling （TUNEL）. The effect of DA on cardiomyocyte ferroptosis were observed and analyzed by in vivo and in vitro experiments. ResultsIn vitro experiment： compared with the blank group， the OGD/R model group showed reduced cell viability， elevated levels of ROS， MDA， and Fe²⁺， up-regulated mRNA and protein levels of ACSL4， lowered levels of SOD and GSH， and down-regulated mRNA and protein levels of PTGS2， GPX4， and FTH1 （P<0.05，P<0.01）. The DA and Fer-1 groups exhibited consistent trends： cell viability， SOD and GSH levels， and the mRNA and protein levels of PTGS2， GPX4， and FTH1 were significantly restored， while the ROS， MDA， and Fe²⁺ levels， and the mRNA and protein levels of ACSL4 were reduced （P<0.05，P<0.01）. In vivo experiment： Compared with the control group， the MIRI model group showed elevated serum levels of cTnI， LDH， and CK， increased cardiomyocyte apoptosis rate， risen levels of ROS， MDA， and Fe²⁺， and up-regulated mRNA and protein levels of ACSL4. However， both DA and Fer-1 groups exhibited reductions in the indicators above （P<0.05）. Compared with the control group， the MIRI model group demonstrated reduced levels of SOD and GSH and down-regulated mRNA and protein levels of PTGS2， GPX4， and FTH1 （P<0.05）. In contrast， both DA and Fer-1 upregulated these indicators （P<0.05）， effectively reversing the trends in the model group. In addition， the MIRI model group showed swelling of cardiomyocytes， disarrangement of cardiac muscle fibers， and massive inflammatory cell infiltration， which were alleviated in the DA and Fer-1 groups. ConclusionDA alleviates MIRI by inhibiting ferroptosis and inflammation， demonstrating therapeutic potential in acute myocardial infarction.

ObjectiveTo investigate the mechanism of danshenol A （DA） pretreatment in alleviating myocardial ischemia-reperfusion injury （MIRI） by regulating cardiomyocyte ferroptosis by in vivo and in vitro experiments. MethodsA MIRI model was established in SD rats， and an in vitro oxygen-glucose deprivation/reoxygenation （OGD/R） model was constructed with H9C2 cells. Both models were treated with DA. H9C2 cells were allocated into blank， model （OGD/R）， DA， ferroptosis inducer （erastin）， and ferroptosis inhibitor （Fer-1） groups. Cell viability was assessed by the methyl thiazolyl tetrazolium （MTT） assay. Biochemical assays were performed to measure the superoxide dismutase （SOD）， malondialdehyde （MDA）， glutathione （GSH）， and ferrous ion （Fe²⁺） levels. Dihydroethidium （DHE） fluorescence assay was adopted to quantify the reactive oxygen species （ROS） level. Real-time PCR and Western blot were employed to quantify the mRNA and protein levels， respectively， of prostaglandin-endoperoxide synthase 2 （PTGS2）， glutathione peroxidase 4 （GPX4）， ferritin heavy chain 1 （FTH1）， and acyl-coA synthetase long-chain family 4 （ACSL4）. Sixty SPF-grade healthy male SD rats were randomly assigned to control， model （MIRI）， DA， erastin， and Fer-1 groups. Enzyme-linked immunosorbent assay （ELISA） was adopted to measure the serum levels of cardiac troponin I （cTnI）， lactate dehydrogenase （LDH）， and creatine kinase （CK）. Histopathological changes in the myocardial tissue were observed by hematoxylin-eosin （HE） staining. Cardiomyocyte apoptosis was detected by terminal deoxynucleotidyl transferase-mediated nick end labeling （TUNEL）. The effect of DA on cardiomyocyte ferroptosis were observed and analyzed by in vivo and in vitro experiments. ResultsIn vitro experiment： compared with the blank group， the OGD/R model group showed reduced cell viability， elevated levels of ROS， MDA， and Fe²⁺， up-regulated mRNA and protein levels of ACSL4， lowered levels of SOD and GSH， and down-regulated mRNA and protein levels of PTGS2， GPX4， and FTH1 （P<0.05，P<0.01）. The DA and Fer-1 groups exhibited consistent trends： cell viability， SOD and GSH levels， and the mRNA and protein levels of PTGS2， GPX4， and FTH1 were significantly restored， while the ROS， MDA， and Fe²⁺ levels， and the mRNA and protein levels of ACSL4 were reduced （P<0.05，P<0.01）. In vivo experiment： Compared with the control group， the MIRI model group showed elevated serum levels of cTnI， LDH， and CK， increased cardiomyocyte apoptosis rate， risen levels of ROS， MDA， and Fe²⁺， and up-regulated mRNA and protein levels of ACSL4. However， both DA and Fer-1 groups exhibited reductions in the indicators above （P<0.05）. Compared with the control group， the MIRI model group demonstrated reduced levels of SOD and GSH and down-regulated mRNA and protein levels of PTGS2， GPX4， and FTH1 （P<0.05）. In contrast， both DA and Fer-1 upregulated these indicators （P<0.05）， effectively reversing the trends in the model group. In addition， the MIRI model group showed swelling of cardiomyocytes， disarrangement of cardiac muscle fibers， and massive inflammatory cell infiltration， which were alleviated in the DA and Fer-1 groups. ConclusionDA alleviates MIRI by inhibiting ferroptosis and inflammation， demonstrating therapeutic potential in acute myocardial infarction.

Myocardial infarction （MI） refers to an acute clinical syndrome of myocardial necrosis due to persistent ischemia and hypoxia， resulting from the sharp reduction or interruption of coronary blood flow. Nuclear factor κB （NF-κB） is the key factor in inducing inflammatory response， and it is involved in the production of pro-inflammatory factors and myocardial cell apoptosis. This article systematically describes the molecular regulation mechanism of the NF-κB signaling pathway in MI， and reviews the related research on the prevention and treatment of MI through the regulation of this signaling pathway by active ingredients and compound formulas from traditional Chinese medicine （TCM）. It has been found that active ingredients from TCM， such as ginsenoside Rg3， baicalein， curcumin， tanshinone ⅡA， gambogic acid， as well as compound formulas， including Qili qiangxin capsules， Yiqi huoxue decoction， Lingbao huxin dan， Danhong injection， Baoyuan decoction combined with Taohong siwu decoction， can improve myocardial fibrosis， alleviate inflammatory responses， and inhibit cardiomyocyte apoptosis by suppressing the NF-κB signaling pathway. Thereby， they achieve the goal of preventing and treating MI.

Myocardial ischemia-reperfusion injury （MIRI） is a major complication following coronary revascularization. Studies indicate that its pathophysiological mechanisms of MIRI are closely associated with oxidative stress， iron overload， inflammatory responses， and lipid peroxidation. Oxidative stress refers to an imbalance in redox homeostasis under pathological conditions， characterized by the abnormal accumulation of reactive oxygen species （ROS）， which disrupts the dynamic balance between pro-oxidant systems and antioxidant defense networks. In recent years， traditional Chinese medicine （TCM） has demonstrated unique advantages in the prevention and treatment of MIRI due to its multi-target and multi-pathway antioxidant properties. Research reveals that TCM primarily exerts protective effects against oxidative stress-induced MIRI by regulating signaling pathways such as nuclear factor erythroid 2-related factor 2 （Nrf2）， adenosine monophosphate-activated protein kinase （AMPK）， phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt）， nuclear factor kappa-B （NF-κB）， Janus kinase 2/signal transducer and activator of transcription 3 （JAK2/STAT3）， and protein kinase C beta Ⅱ/nicotinamide adenine dinucleotide phosphate oxidase 2/reactive oxygen species （PKCβⅡ/NOX2/ROS）. This article reviews recent literature on TCM monomers， compound formulas， and their active components， which alleviate oxidative stress to prevent and treat MIRI by modulating the aforementioned signaling pathways. It summarizes a concise overview of the molecular mechanisms by which oxidative stress-related signaling pathways lead to MIRI， discusses how TCM regulates these pathways to reduce oxidative stress-induced MIRI， and explores clinical application prospects and research challenges， aiming to provide a theoretical reference for the research and clinical management of MIRI.

Background Maternal exposure to bisphenol A (BPA) during pregnancy is closely related to adverse growth and development conditions such as preterm birth and low birth weight, but the relevant mechanisms are still unclear. UDP-glucuronosyltransferases (UGTs) can regulate the excretion of BPA conjugating with glucuronic acid through urine, which is one of the important pathways for BPA elimination. Objective To explore the changes in the expression of UGTs in placenta and fetal liver of rats before birth induced by maternal exposure to BPA during pregnancy. Methods Thirty SPF-grade healthy SD pregnant rats were randomly divided into five groups: control group, 0.05, 0.5, 5, and 50 mg·kg⁻¹ BPA groups. The pregnant rats were exposed to BPA dissolved in corn oil via oral gavage daily from gestational day (GD) 5 to GD 19. After anesthesia, the pregnant rats were sacrificed on GD 20 and the placentas were collected. Body length, tail length, and weight of the fetal rats were measured. Fetal liver tissues were then separated, and organ weights were measured. Real-time quantitative polymerase chain reaction (RT-PCR) and Western blot (WB) were used to determine the mRNA and protein levels of UGT1A1, UGT1A6, UGT1A9, and UGT2B1 in the placenta and fetal liver tissues in each group. Results There were no differences in body length and tail length of the pups after maternal exposure to BPA during pregnancy. The fetal body weight and placenta weight in the 5 and 50 mg·kg⁻¹ BPA groups and the liver weight in the 5 mg·kg⁻¹ BPA group reduced compared with the control group (P<0.05). The results of UGTs expressions in placenta showed that compared with the control group, the UGT1A1 mRNA levels in placenta of the BPA groups (exposure dose≥0.5 mg·kg⁻¹) and the UGT1A1 protein level in placenta of the 50 mg·kg⁻¹ BPA group increased (P<0.05); the UGT1A6 mRNA and protein levels in placenta of each BPA group did not change (P>0.05); the UGT1A9 mRNA level in placenta of the 50 mg·kg⁻¹ BPA group and the UGT1A9 protein levels in placenta of the BPA groups (exposure dose≥0.5 mg·kg⁻¹) reduced (P<0.05); while the levels of UGT2B1 mRNA in placenta of the BPA groups (exposure dose≥0.5 mg·kg⁻¹) reduced (P<0.05). The results of UGTs expressions in fetal liver showed that compared with the control group, the UGT1A1, UGT1A6, UGT1A9, and UGT2B1 mRNA levels of each BPA group increased (P<0.05); no obvious alternation was observed in UGT1A6 protein levels in each BPA group (P>0.05); the relative protein levels of UGT1A9 in fetal liver in the 50 mg·kg⁻¹ BPA group increased (P<0.05); conversely, the relative protein levels of UGT2B1 in fetal liver in the BPA groups (exposure dose≥0.5 mg·kg⁻¹) reduced (P<0.05). Conclusion Maternal exposure to BPA during pregnancy can elevate the UGT1A1 gene and protein expressions, inhibit the UGT1A9 gene and protein expressions and UGT2B1 gene expressions in placenta. Besides, maternal exposure to BPA during pregnancy can raise the gene expressions of UGT1A1, UGT1A6, UGT1A9, and UGT2B1 in fetal liver, as well as the protein expression of UGT1A9, but inhibit the protein expression of UGT2B1. These changes may contribute to fetal developmental abnormalities after maternal exposure to BPA during pregnancy.

Objective To evaluate the bidirectional association between periodontitis and Sj?gren's syndrome us-ing the Mendelian randomization(MR)method.Methods Genome-wide association study(GWAS)data of periodonti-tis(N=45 563)and Sj?gren's syndrome(N=214 435)were selected to meet the requirements of the same ethnicity and different regions.Inverse variance-weighted(IVW),MR-Egger,and weighted median(WM)tests were used to evalu-ate the causal effect.Cochran's Q statistics,MR-Egger intercept,MR-PRESSO and leave-one-out analysis were used as sensitivity analyses to assess the stability and reliability of the results.Results After screening,the GWAS data of Sj?gren's syndrome were based on the Finnish region,and the periodontitis GWAS data were based on the UK region,both of which originated from European ancestry.Using IVW(OR=1.017,95％CI=0.956-1.082),MR-Egger(OR=0.985,95％CI=0.956-1.082),and WM(OR=1.021,95％CI=0.948-1.099),no causal effect of Sj?gren's syndrome on periodontitis was found using any of the three methods.Conversely,no causal effect of periodontitis on Sj?gren s syn-drome was found(IVW,OR=1.024,95％CI=0.852-1.230;MR-Egger,OR=0.978,95％CI=0.789-1.212;WM,OR=1.024,95％CI=0.846-1.260).The sensitivity analyses indicated that the results were stable and reliable.Cochran's Q test and MR-PRESSO revealed that there was no significant heterogeneity among the instrumental variables,which included single nucleotide polymorphisms(SNPs).The intercept of MR-Egger regression indicated no pleiotropy in the included SNPs.No individual SNP was found that significantly affected the results using the leave-one-out method.Conclusion This study does not support a bidirectional causal effect between periodontitis and Sj?gren's syndrome.

Objective To evaluate the bidirectional association between periodontitis and Sj?gren's syndrome us-ing the Mendelian randomization(MR)method.Methods Genome-wide association study(GWAS)data of periodonti-tis(N=45 563)and Sj?gren's syndrome(N=214 435)were selected to meet the requirements of the same ethnicity and different regions.Inverse variance-weighted(IVW),MR-Egger,and weighted median(WM)tests were used to evalu-ate the causal effect.Cochran's Q statistics,MR-Egger intercept,MR-PRESSO and leave-one-out analysis were used as sensitivity analyses to assess the stability and reliability of the results.Results After screening,the GWAS data of Sj?gren's syndrome were based on the Finnish region,and the periodontitis GWAS data were based on the UK region,both of which originated from European ancestry.Using IVW(OR=1.017,95％CI=0.956-1.082),MR-Egger(OR=0.985,95％CI=0.956-1.082),and WM(OR=1.021,95％CI=0.948-1.099),no causal effect of Sj?gren's syndrome on periodontitis was found using any of the three methods.Conversely,no causal effect of periodontitis on Sj?gren s syn-drome was found(IVW,OR=1.024,95％CI=0.852-1.230;MR-Egger,OR=0.978,95％CI=0.789-1.212;WM,OR=1.024,95％CI=0.846-1.260).The sensitivity analyses indicated that the results were stable and reliable.Cochran's Q test and MR-PRESSO revealed that there was no significant heterogeneity among the instrumental variables,which included single nucleotide polymorphisms(SNPs).The intercept of MR-Egger regression indicated no pleiotropy in the included SNPs.No individual SNP was found that significantly affected the results using the leave-one-out method.Conclusion This study does not support a bidirectional causal effect between periodontitis and Sj?gren's syndrome.

Objective To evaluate the bidirectional association between periodontitis and Sj?gren's syndrome us-ing the Mendelian randomization(MR)method.Methods Genome-wide association study(GWAS)data of periodonti-tis(N=45 563)and Sj?gren's syndrome(N=214 435)were selected to meet the requirements of the same ethnicity and different regions.Inverse variance-weighted(IVW),MR-Egger,and weighted median(WM)tests were used to evalu-ate the causal effect.Cochran's Q statistics,MR-Egger intercept,MR-PRESSO and leave-one-out analysis were used as sensitivity analyses to assess the stability and reliability of the results.Results After screening,the GWAS data of Sj?gren's syndrome were based on the Finnish region,and the periodontitis GWAS data were based on the UK region,both of which originated from European ancestry.Using IVW(OR=1.017,95％CI=0.956-1.082),MR-Egger(OR=0.985,95％CI=0.956-1.082),and WM(OR=1.021,95％CI=0.948-1.099),no causal effect of Sj?gren's syndrome on periodontitis was found using any of the three methods.Conversely,no causal effect of periodontitis on Sj?gren s syn-drome was found(IVW,OR=1.024,95％CI=0.852-1.230;MR-Egger,OR=0.978,95％CI=0.789-1.212;WM,OR=1.024,95％CI=0.846-1.260).The sensitivity analyses indicated that the results were stable and reliable.Cochran's Q test and MR-PRESSO revealed that there was no significant heterogeneity among the instrumental variables,which included single nucleotide polymorphisms(SNPs).The intercept of MR-Egger regression indicated no pleiotropy in the included SNPs.No individual SNP was found that significantly affected the results using the leave-one-out method.Conclusion This study does not support a bidirectional causal effect between periodontitis and Sj?gren's syndrome.

Objective To evaluate the bidirectional association between periodontitis and Sj?gren's syndrome us-ing the Mendelian randomization(MR)method.Methods Genome-wide association study(GWAS)data of periodonti-tis(N=45 563)and Sj?gren's syndrome(N=214 435)were selected to meet the requirements of the same ethnicity and different regions.Inverse variance-weighted(IVW),MR-Egger,and weighted median(WM)tests were used to evalu-ate the causal effect.Cochran's Q statistics,MR-Egger intercept,MR-PRESSO and leave-one-out analysis were used as sensitivity analyses to assess the stability and reliability of the results.Results After screening,the GWAS data of Sj?gren's syndrome were based on the Finnish region,and the periodontitis GWAS data were based on the UK region,both of which originated from European ancestry.Using IVW(OR=1.017,95％CI=0.956-1.082),MR-Egger(OR=0.985,95％CI=0.956-1.082),and WM(OR=1.021,95％CI=0.948-1.099),no causal effect of Sj?gren's syndrome on periodontitis was found using any of the three methods.Conversely,no causal effect of periodontitis on Sj?gren s syn-drome was found(IVW,OR=1.024,95％CI=0.852-1.230;MR-Egger,OR=0.978,95％CI=0.789-1.212;WM,OR=1.024,95％CI=0.846-1.260).The sensitivity analyses indicated that the results were stable and reliable.Cochran's Q test and MR-PRESSO revealed that there was no significant heterogeneity among the instrumental variables,which included single nucleotide polymorphisms(SNPs).The intercept of MR-Egger regression indicated no pleiotropy in the included SNPs.No individual SNP was found that significantly affected the results using the leave-one-out method.Conclusion This study does not support a bidirectional causal effect between periodontitis and Sj?gren's syndrome.

[Objective] To investigate the clinical manifestations and explore the experience of diagnosis and treatment of spontaneous perirenal urine extravasation after urinary tract obstruction so as to improve the understanding of the disease. [Methods] The clinical data of 23 patients with spontaneous perirenal urine extravasation after obstruction treated at our hospital during 2018 and 2020 were retrospectively analyzed, including the primary diseases, clinical manifestations, imaging examination, treatment and prognosis. The key points of diagnosis and treatment were summarized. [Results] Of the 23 patients, there were 15 males and 8 females, with an average age of 43.4 years. These cases were diagnosed by imaging tests such as ultrasound, computed tomography urography (CTU) and CT. Ureteroscopic lithotripsy was performed in 3 patients with ureteral calculi, retrograde ureteral catheterization in 4 patients and percutaneous nephrostomy in 13 patients. Afterwards, a second phase surgery was performed based on the patients' condition. Of the 3 patients with tumor metastasis who underwent retrograde ureteral catheterization, 2 operation were successful, and 1 operation failed and then converted to nephrostomy and drainage under B-ultrasound localization. [Conclusion] CTU should be performed as soon as possible to make a definite diagnosis. Treatment can be achieved with ureteral retrograde catheterization or percutaneous nephrostomy to achieve local decompression, followed by secondary surgery to treat the primary cause of obstruction.