Objective To investigate the dynamics of the level of S100 in cerebrum, brainstem, and serum following the diffuse brain injury in rats and provide the experimental evidences for estimating injury time. Methods ELISA was used to determine whether S100 protein is changed after diffuse brain injury in rats. Forty rats were sacrificed at 0.5 hour, 2 hours, 4 hours, 12 hours, 24 hours, 3 d and 7 d after diffuse brain injury and normal rats as control. Results The level of S100 in cerebrum, brainstem, and serum increased, followed by a decrease, and then further increased. The level of S100 could be detected to increase at 30 minutes and reached the peak at 4 hours after DBI. The level decreased gradually to the normal at 1d and till 3 d formed the second peak. The level returned to the normal at 7d following injury again. In the postmortem injury groups, there were no significant changes compared to the control group. Conclusion The present study showed that the time-dependent expression of S100 is obvious following diffuse brain injury in rats and suggested that S100 will be a suitable marker for diffuse brain injury age determination.

OBJECTIVETo investigate the expression change of matrix metalloproteinase-9 (MMP-9) and nuclear factor-kappaB (NF-kappaB) induced by Xuemaitong capsule (XMT) preconditioning on rats of myocardial ischemia, and provide experimental evidence for the protection of XMT.

METHOD60 wistar rats were randomly divided into 5 roups: the control group, the model group, the three difference dose groups of XMT. The groups of XMT were treated by continuous 14 days intragastric administration. After 14 days, except the control group, all groups were continuous 2 days subcutaneous injected with isoproterenol 30 mg x kg(-1) every day. Before and 5, 10, 20, 30 minutes after subcutaneous injection, electrocardiogram were recorded, immunohistochemical staining, RT-PCR and image analysis were also measured for the investigation of the expression of MMP-9 and NF-KB in the ischemic region.

RESULTCompared with the model group, the delta sigma-ST of electrocardiogram of the high dose, middle dose, low dose groups of XMT decreased at different degree. Pathological conditions of ischemic myocardial ameliorated. The immunohistochemical staining and RT-PCR indicated that the expression of MMP-9 and NF-kappaB decreased in the high dose group (P < 0.05), the mRNA expression of MMP-9 and NF-kappaB decreased in the high dose group (P < 0.05).

CONCLUSIONThe expression of MMP-9 and NF-kappaB increased after myocardial ischemia After high dose treated by XMT, the expression reduction of MMP-9 and NF-kappaB indicated that XMT played an important preventive role in acute myocardial ischemia.

Animals ; Capsules ; Disease Models, Animal ; Down-Regulation ; drug effects ; Drugs, Chinese Herbal ; administration & dosage ; Female ; Gene Expression ; drug effects ; Humans ; Male ; Matrix Metalloproteinase 9 ; genetics ; metabolism ; Myocardial Ischemia ; drug therapy ; genetics ; metabolism ; prevention & control ; NF-kappa B ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Wistar

Objective To systematically evaluate the medication experience of patients with chronic multimorbidities and to provide a reference for developing precise intervention programs to improve the medication experience of patients with chronic multimorbidities.Methods PubMed,Cochrane Library,Web of Science,Embase,CINAHL,PsycINFO,CNKI,Wanfang database,VIP database,and Chinese biomedical literature database were searched from the year of database establishment to October 2022,and qualitative studies on medication experiences of patients with chronic multimorbidities were retrieved.The Joanna Briggs Institute Critical Appraisal Tool for qualitative research(2016)in Australia was used to evaluate quality of the studies.A meta-synthesis method was used to integrate the results.Results A total of 11 articles were included,and 56 research results were extracted and integrated into 12 new categories,which were summarized into 4 integrated results:poor sensory experience of drugs,negative emotional and related experiences,reflective and behavioral experiences,and multi-dimensional debugging to improve medication experience.Conclusion The medication experience of patients with chronic multimorbidities should receive extensive attention from society and medical workers,and future research should be conducted to improve the level of patients'medication experience in 5 dimensions,including sensory experience,emotional experience,reflective experience,behavioral experience and associative experience,so as to provide a basis for further improving the medication experience of patients with chronic multimorbidities in China.

Objective To evaluate the effect of α7 nicotinic acetylcholine receptor (α7nAChR)agonists on lung injury caused by cardiopulmonary bypass (CPB) in rats.Methods Eighteen healthy clean-grade adult male Sprague-Dawley rats,weighing 350-400 g,were divided into 3 groups (n =6 each)using a random number table method:sham operation group (group S),CPB group and α7nAChR agonist PHA568487 group (group PHA).The rats underwent no CPB and were mechanically ventilated for 60 min in group S.PHA568487 0.8 mg/kg (diluted to 2 ml in normal saline) was intraperitoneally injected at 30 min before CPB,and then CPB was performed for 60 min in group PHA.Normal saline 2 ml was intraperitoneally injected at 30 min before CPB,and then CPB was performed for 60 min in group CPB.Blood samples were collected from the internal jugular vein for determination of serum interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) concentrations by enzyme-linked immunosorbent assay.Lung tissues were obtained for microscopic examination of the pathologic changes and for determination of wet/dry weight ratio (W/D ratio) and matrix metalloproteinase-9 (MMP-9) expression (by Western blot).Results Compared with group S,the W/D ratio and serum concentrations of TNF-α and IL-6 were significantly increased,and the expression of MMP-9 was up-regulated in CPB and PHA groups (P＜0.05).Compared with group CPB,the W/D ratio and serum concentrations of TNF-α and IL-6 were significantly decreased,the expression of MMP-9 was down-regulated (P＜0.05),and the pathological changes of lung tissues were significantly attenuated in group PHA (P＜0.05).Conclusion α7nAChR agonists can reduce the acute lung injury caused by CPB in rats,and the mechanism may be related to down-regulating MMP-9 expression and inhibiting systemic inflammatory responses.

Objective To investigated the effect of tripterygium glycosides(TG)on dextran sodium sulfate(DSS)-induced colonic mucosal damage in ulcerative colitis(UC)mice and its regulatory mechanism.Methods Forty C57BL/6J mice were randomly divided into a normal group,a model group,and a tretinoin low,medium,and high dose group(administered at concentrations of 9.00mg/kg,27.03mg/kg,and 81.09mg/kg,respectively).The mice in the normal group were free to drink distilled water,and the rest of the mice drank 5％DSS to induce UC modeling.After modeling,mice in the model group were given 0.4ml of saline by gavage daily,and the rest of the mice in the treatment group were given the corresponding dose of TG for gavage intervention.The mass and disease activity index of the mice in each group were compared,and the pathological and histological damage of the colon was observed.Tumor necrosis factor-α(TNF-α),malondialdehyde(MDA),and superoxide dismutase(SOD)levels were measured using the corresponding kits.Western blot Detection of Nur77,tumor necrosis factor receptor-associated factor 2(Traf2),nucleoporin 62(P62),autophagy protein-microtubule associated protein1 light chain 3(LC3)molecular expression.Results Compared with the blank group,the body weight,colon length,SOD,Nur77,Traf2,and LC3Ⅱ/LC3Ⅰ levels of mice in the model group were significantly decreased(P<0.05),and the DAI level,colon pathology score,TNF-α,MDA level,and P62 of the mice were significantly increased(P<0.05).Compared with mice in the UC model group,mice in the low,medium and high dose groups of tretinoin polyphenols showed significant increases in body weight,colon length,SOD,Nur77,Traf2,LC3Ⅱ/LC3Ⅰlevels(P<0.05),and mice with DAI scores,TNF-α,MDA levels in the colon,and P62 levels were significantly decreased(P<0.05).Mice in the medium and high dose groups of tretinoin polyphenols pathological scores were significantly reduced(P<0.05).Conclusion TG is able to treat ulcerative colitis through Nur77-Traf2-P62 signaling pathway.