Protective effect of liraglutide on the myocardium of type 2 diabetic rats by inhibiting polyadenosine diphosphate-ribose polymerase-1

BACKGROUND In recent years,studies have found that the occurrence and development of diabetic cardiomyopathy(DCM)is closely related to an increase in polyadenosine diphosphate-ribose polymerase-1(PARP-1)activity.PARP-1 activation could be involved in the pathophysiological process of DCM by promoting oxidative stress,the inflammatory response,apoptosis and myocardial fibrosis.AIM To investigate the mechanism of liraglutide in improving myocardial injury in type 2 diabetic rats,further clarified the protective effect of liraglutide on the heart,and provided a new option for the treatment of DCM.METHODS Forty healthy male SD rats aged 6 wk were randomly divided into two groups,a normal control group(n=10)and a model group(n=30),which were fed an ordinary diet and a high-sugar and high-fat diet,respectively.After successful modeling,the rats in the model group were fed a high-glucose and high-fat diet for 4 wk and randomly divided into a model group and an intervention group(further divided into a high-dose group and a low-dose group).The rats were fed a high-glucose and high-fat diet for 8 wk and then started drug intervention.Blood samples were collected from the abdominal aorta to detect fasting blood glucose and lipid profiles.Intact heart tissue was dissected,and its weight was used to calculate the heart weight index.Haematoxylin and eosin staining was used to observe the pathological changes in the myocardium and the expression of PARP-1 in the heart by immunohistochemistry.RESULTS The body weight and heart weight index of rats in the model group were significantly increased compared with those in the normal control group,and those in the intervention group were decreased compared with those in the model group,with a more obvious decrease observed in the high-dose group(P<0.05).In the model group,myocardial fibers were disordered,and inflammatory cells and interstitial fibrosis were observed.The cardiomyopathy of rats in the intervention group was improved to different degrees,the myocardial fibers were arranged neatly,and the myocardial cells were clearly striated;the improvement was more obvious in the high-dose group.Compared with the normal control group,the expression of PARP-1 in myocardial tissue of the model group was increased,and the difference was statistically significant(P<0.05).After liraglutide intervention,compared with the model group,the expression of PARP-1 in myocardial tissue was decreased,and the reduction was more obvious in the high-dose group(P<0.05)but still higher than that in the normal control group.CONCLUSION Liraglutide may improve myocardial injury in type 2 diabetic rats by inhibiting the expression of myocardial PARP-1 in a dose-dependent manner.

Collagenous gastritis in a young Chinese woman:A case report

BACKGROUND Collagenous gastritis(CG) is a rare condition whose pathogenesis may be related to immune abnormalities. We report a case of CG from China.CASE SUMMARY A 24-year-old woman presented with recurrent abdominal distension and discomfort for 3 mo. Upper gastrointestinal endoscopy found diffuse nodular elevation-depression changes in the mucosa of the entire gastric corpus.Endoscopic ultrasound showed predominant involvement of the lamina propria and submucosa, and computed tomography imaging showed mild enhancement of the gastric wall. Pathological histology revealed that the thickness of the subepithelial collagen band was about 40 μm, and the Masson trichrome staining result was positive and the Congo red staining result was negative. This case is consistent with the child-adolescent type of CG.CONCLUSION Serum pepsinogen Ⅰ, pepsinogen Ⅱ, pepsinogen Ⅰ/Ⅱ ratio, and gastrin-17 may be potential non-invasive monitoring markers. Currently, treatments for CG vary,and the likely prognosis is unknown. Individual cases of gastric cancer in patients with CG have been reported.

Electroacupuncture regulates the stress-injury-repair chain of events after cerebral ischemia/reperfusion injury

Inflammation after stroke is the main cause of cerebral ischemia/reperfusion injury. Cascading events after injury can lead to cell death. Heat shock protein 70 and other endogenous injury-signaling molecules are released by damaged cells, which can lead to systemic stress reactions. Protecting the brain through repair begins with the stress-injury-repair signaling chain. This study aimed to verify whether acupuncture acts through this chain to facilitate effective treatment of ischemic stroke. Rat models of cerebral ischemia/reperfusion injury were established by Zea Longa＇s method, and injury sites were identified by assessing neurological function, 2,3,5-triphenyltetrazolium chloride staining, and hematoxylin-eosin staining. Electroacupuncture at acupoints Baihui（DU20） and Zusanli（ST36） was performed in the model rats with dilatational waves, delivered for 20 minutes a day at 2–100 Hz and an amplitude of 2 m A. We analyzed the blood serum from the rats and found that inflammatory cytokines affected the levels of adrenotrophin and heat shock protein 70, each of which followed a similar bimodal curve. Specifically, electroacupuncture lowered the peak levels of adrenocorticotrophic hormone and heat shock protein 70. Thus, electroacupuncture was able to inhibit excessive stress, reduce inflammation, and promote the repair of neurons, which facilitated healing of ischemic stroke.

The study of selective primary culture and determination of a breast cancer cell line in vitro

Objective The successful establishment of a tumor cell bank is based on the premise that the target cells can be cultured by a legitimate approach.In this experiment,we used primary culture to select and detect breast cancer cells in vitro,which can provide experimental ideas and methods for the establishment of a living tumor tissue cell bank.Methods Fifty-two specimens were collected over a two-year period from people with breast cancer who needed surgical treatment in our hospital.Cells were isolated and used to establish successful cell culture.Cell activity and cell purity were measured before liquid nitrogen cryopreservation.Results(1)At the initial culture stage,cells grew with adherence.Cell multiplication could be seen after the cell medium was exchanged three times.Cell viability was above 86%,while the viability of the target cells was above 75%,as detected by hematoxylin and eosin(HE)staining.(2)The number of breast cancer cells decreased,while the number of fibroblasts increased after five rounds of passage.(3)The success rate was 73.08%,which did not include polluted cells and those that were not successfully cryopreserved.Conclusion(1)breast cancer cells could be selected from primary culture in vitro through an appropriate method.(2)Exchange of the cell medium and further cell passage improved cell multiplication.(3)The experimental results could be monitored using trypan blue and HE staining.(4)The success of breast cancer cell culture in vitro could be used as a reference for other cell culture,so as to establish a tumor tissue cell bank.

Isoprenaline increases serum levels of monocyte chemoattractant protein-1 and tissue inhibitor of matrix metalloproteinases type I in Wistar rats

Background Treatment of rats with the beta-adrenergic agonist Isoprenaline（ISO） results in cardiac hypertrophy and myocardial fibrosis.In the present work,we aimed to study the in vivo effects of ISO on serum levels of monocyte chemoattractant protein- 1 and tissue inhibitor of matrix metalloproteinases type I in Wistar rats.Methods ISO（5 mg·kg-1） or Saline were injected subcutaneously into Wistar rats once a day for 3 or 7 consecutive days.Ventricular remodeling and cardiac function were evaluated by echocardiography.Sections of heart were stained with hematoxylin-eosin（HE） for histopathology or with Massons trichrome for collagen visualization.In addition,heart tissue immunohistochemistry for ɑ-SMA was also analyzed.The serum levels of tissue inhibitor of matrix metalloproteinases type I（TIMP-1） and monocyte chemoattractant protein-1（MCP-1） were determined by Luminex multiplex technology.Results ISO induced cardiac dysfunction in rats after 3 or 7 days of treatment.ISO caused significant increase of myocardial disorder and fibrosis withincreased ɑ-SMA expression.ISO treated aats showed a significant increase in the serum levels of TIMP- 1 and MCP-1.Conclusions Our study suggests that ISO induces profound cardiac remodeling accompanied with increase of serum TIMP-1and MCP-1.