Purpose Medicine information and features of adverse reactions induced by non-ionic iodinated contrast agent injection for CT examination are analyzed and discussed,offering empirical evidence and reference for medication choice and patient information for clinical CT examination and targeted adverse reactions disposal.Materials and Methods General material,medicine type and name,adverse reactions occurrence time,symptoms and other information of the 20,418 patients receiving CT examination with non-ionic iodinated contrast agent at X-ray Department in Gansu Provincial Hospital from July 2013 to September 2016 were retrospectively analyzed.Results For observation objects in this group,11,679 were male and 8,739 female,aging from 3 to 93 and the average age was (52.1 ± 13.2) years.Various adverse reactions occurrence rate of non-ionic iodinated contrast agent was 0.4％ and adverse reactions occurrence rate of secondary hypertonic contrast and isotonic contrast agent was 0.47％ and 0.27％,respectively.Among the 81 adverse reactions,91.3％ were acute,among which 88.9％ occurred within 15 min after injection.8.7％ were delayed,97.6％ mild and moderate,and 2.4％ severe.Secondary hypertonic contrast and isotonic contrast agent occupied 74.0％ and 26.0％,respectively for the cause of adverse reactions.Delayed adverse reactions were mainly caused by isotonic contrast agent,representing as mild and moderate.Representation frequency of adverse reactions symptoms in turn was skin,digestive tract,central nervous system,respiratory system and circulatory system.Conclusion Adverse reactions caused by iodinated contrast agent were mainly acute and mild and moderate.The patients or their family members shall be fully notified before examinations.Severe adverse reactions caused by iodinated contrast agent developed very quickly and multi-systems would be damaged.Efficient on-site treatment is very important.Delayed reactions caused by isotonic contrast agent shall be paid more attention.

Post-stroke cognitive impairment (PSCI), one of the important complications of stroke, seriously affects the quality of life of these patients. PSCI is an important cause of disease burden of stroke. In recent years, more and more evidences show that blood biomarkers are of great significance in PSCI diagnosis, and the detection of blood biomarkers is relatively simple and more suitable for clinical application. Therefore, this paper sorts out the values of 5 blood biomarkers, nerve injury marker, metabolic biomarker, inflammatory biomarker, oxidative stress marker and other biomarker, in diagnosing PSCI, to provide references for early diagnosis and intervention of PSCI.

OBJECTIVE To investigate the regulatory effects of icariin(ICA)on cardiac micro-vascular endothelial cells(CMEC)after oxygen-glucose deprivation reperfusion(OGD/R)injury.METHODS CMEC were subjected to OGD/R treatment to construct a myocardial ischemia-reperfusion model,and were divided into normal,model,low(10 μmol·L-1),medium(20 μmol·L-1)and high(40 μmol·L-1)ICA group,and high ICA+ inhibitor group(40 μmol·L-1+20 nmol·L-1).CCK-8 assay was used to assess the protective ability of ICA against CMEC,and cell migration assay and tube-formation assay were used to detect the migration and generation ability of CMEC.The TCMSP database,Swiss-Target database and literature mining methods were used to col-lect ICA-related targets,the GeneCards data-base was used to collect target genes related to myocardial ischemia/reperfusion,and Cytoscape 3.8.0 software was used to construct a"drug-tar-get-disease"network.The potential targets were imported into STRING 11.5 database to obtain the PPI network.GO and KEGG enrichment analyses were performed on the potential targets using the DAVID database.Molecular docking was performed using AutoDock-vina 1.1.2 soft-ware.Western blot detected the expression of related proteins.RESULTS After CMEC was subjected to OGD/R treatment,ICA had a protec-tive effect at 10-160 μmol·L-1;the results of the cell migration assay showed that each group of ICA could promote the migratory effect of CMEC(P＜0.01,P＜0.01);and the results of tube-for-mation assay showed that each group of ICA could significantly promote the generation of branches(P＜0.01)and the capillary length exten-sion(P＜0.05).Network pharmacology collected a total of 23 ICA action targets,1500 disease tar-gets and 12 key targets.GO function enrichment analysis found 85 results.KEGG pathway enrich-ment analysis found 53 results,involving AGE-RAGE signaling pathway,sphingolipid signaling pathway and VEGF signaling pathway.Molecu-lar docking results showed that ICA had better binding with core targets PRKCB,PRKCA and PTGS2.Western blot results showed that ICA could regulate the expression of PRKCB,PRKCA and PTGS2 proteins.The results of cell migra-tion assay,tube-formation assay and protein expression were reversed after addition of PKC inhibitor.CONCLUSION The potential mecha-nism of action of ICA against myocardial isch-emia-reperfusion injury may be related to the reg-ulation of processes such as CMEC migration and angiogenesis,and it functions through the key target gene PKC.

Ferroptosis is a new type of programmed cell death， characterized by iron overload and lipid peroxidation. Cardiovascular disease （CVD） is an ischemic or hemorrhagic disease of the heart caused by various factors， mainly including myocardial infarction， heart failure， etc. Ferroptosis is involved in the process of myocardial cell damage and plays a driving role in the progression of various CVDs. Its main mechanisms include the destruction of iron homeostasis， the production of reactive oxygen species， the disorder of the antioxidant system， mitochondrial membrane damage， endoplasmic reticulum stress， tumor suppressor gene p53， transcription factor Nrf2 pathway， etc. Myocardial injury is one of the causes of death in many patients with heart disease. Monomers or compounds of traditional Chinese medicine have shown good effects in the treatment of myocardial cell injury caused by ferroptosis， including baicalin protecting cardiac microvascular endothelial cells of myocardial ischemia-reperfusion （I/R） rats through intracellular phosphatidylinositol kinase/phosphokinase B/endothelial nitric oxide synthase （PI3K/Akt/eNOS） pathway， Aralia elata saponin inhibiting myocardial cell ferroptosis through glucocorticoid receptor/p53/solute carrier family 7 members 11 （NR3C1/p53/SLC7A11） pathway， Xinyang tablets improving oxidative stress by regulating phosphorylated serine/threonine protein kinase/stress-activated protein kinase/p53 （MLK3/JNK/p53） signaling pathway. It is of great significance to explore the mechanism of ferroptosis and the protective effect of related traditional Chinese medicine after myocardial cell injury. This article reviews the mechanism of ferroptosis and its relationship with myocardial cells， as well as traditional Chinese medicine monomers and formulas for treating CVDs through the ferroptosis pathway. The article focuses on the pathways and effects of traditional Chinese medicine treatment， so as to provide a reference for the treatment of CVDs with traditional Chinese medicine.

ObjectiveTo observe and compare the electrocardiogram index， myocardial morphology， and connexin 43 （Cx43） expression of two rat models of acute cerebral infarction （ACI） due to stasis combined with toxin complicated with cerebral-cardiac syndrome （CCS）， and to provide experimental evidence for the research on the occurrence mechanism of cardiac diseases induced by ACI and the clinical diagnosis and treatment of CCS. MethodSixty SPF-grade male SD rats were randomized into six groups （n=10）： normal ， syndrome of stasis combined with toxin induced by carrageenin combined with dry yeast （CA/Y）， multi-infarct induced by micro-embolism （ME）， middle cerebral artery occlusion （MCAO）， CA/Y+ME， and CA/Y+MCAO groups. The model of syndrome of stasis combined with toxin was established by intraperitoneal injection with carrageenan （CA） at 10 mg·kg^-1 on the first day and subcutaneous injection with dry yeast （Y） suspension （2 mg·kg^-1） on the second day of modeling. Twenty-four hours after the modeling of ACI， the electrocardiograms （ECGs） of rats in each group were collected and the number/percentage （%） of abnormal ECG was calculated. The infarct area of the brain was evaluated by 2，3，5-triphenyltetrazolium chloride （TTC） staining， and myocardial injury was assessed by hematoxylin-eosin （HE） staining. Immumohistochemical staining and Western blot were employed to determine the expression of Cx43 in the myocardium. ResultA certain number of rats in each model group presented abnormal ECG. Compared with the normal group and CA/Y group， CA/Y+MCAO group had the highest rate of abnormal ECG （P<0.01）. Compared with the normal， CA/Y， ME， and CA/Y+ME groups， the CA/Y+ME and CA/Y+MCAO groups showed decreased amplitudes of P-wave and T-wave， shortened P-R interval， and extended Q-T interval， which were particularly obvious in the CA/Y+MCAO group （P<0.05， P<0.01） and in accordance with the cerebral infarction area and pathological changes. The expression of Cx43 was up-regulated in both CA/Y+ME and CA/Y+MCAO groups， especially in the CA/Y+MCAO group （P<0.01）. ConclusionThe two rat models of ACI due to stasis combined with toxin complicated with CCS can be used to study the mechanism of heart diseases caused by cerebrovascular diseases and the therapeutic effects of Chinese medicines with the functions of resolving stasis and detoxifying. Moreover， the CA/Y+MCAO method has higher abnormal electrocardiogram rate， severer myocardial pathological injury， and higher expression of Cx43 protein. The models can be chosen according to specific experimental purpose.

ObjectiveTo explore whether the mechanism of Shuangshen Ningxin capsules （SSNX） in alleviating myocardial ischemia-reperfusion injury （MIRI） in rats is related to the regulation of mitochondrial fission and fusion. MethodThis study focused on Sprague Dawley （SD） rats and ligated the left anterior descending branch of the coronary artery to construct a rat model of MIRI. The rats were divided into the sham operation group， model group， SSNX group （90 mg·kg^-1） and trimetazidine group （5.4 mg·kg^-1）. The activity of superoxide dismutase （SOD） and the content of malondialdehyde （MDA） were detected by micro method. Changes in mitochondrial membrane potential （△Ψm） and the degree of mitochondrial permeability transition pore （mPTP） opening were detected by the chemical fluorescence method. The intracellular adenosine triphosphate （ATP） level was detected by the luciferase assay. The messenger ribonucleic acid （mRNA） and protein expression levels of mitochondrial fission and fusion related factors dynamin-related protein 1 （DRP1）， mitochondrial fission 1 protein （FIS1）， optic atrophy protein 1 （OPA1）， mitochondrial outer membrane fusion protein 1 （MFN1）， and MFN2 were detected by real-time polymerase chain reaction （real-time PCR） and Western blot. ResultCompared with the sham operation group， the model group showed a decrease in serum SOD activity and an increase in MDA content. The opening level of mPTP， the level of △Ψm and ATP content decreased， the protein expressions of mitochondrial fission factors DRP1 and FIS1 increased， and the protein expressions and mRNA transcription levels of fusion related factors OPA1 and MFN1 decreased. Compared with the model group，SSNX significantly increased serum SOD activity， reduced MDA content， increased intracellular ATP level and △Ψm， reduced the opening level of mPTP， downregulated the protein expressions of mitochondrial fission factors DRP1 and FIS1， and increased the mRNA transcription levels and protein expressions of fusion related factors OPA1 and MFN1. ConclusionSSNX inhibits the expressions of mitochondrial fission factors DRP1 and FIS1， and increases the expressions of fusion related factors OPA1 and MFN1， inhibiting mitochondrial fission and increasing mitochondrial fusion， thereby alleviating MIRI.