Aim To study the protective effect and mechanism of geniposide on human umbilical vein endothelial cell(HUVEC) injury induced by H2O2.Methods The injured model was established by HUVEC treated with H2O2.HUVECs were cultured in vitro and divided into five groups:control group,H2O2 group and geniposide with different concentrations plus H2O2 group respectively.HUVECs were incubated with 400 ?mol?L-1 H2O2 for 12 hours in the absence or presence of various concentrations of geniposide pre-incubation.Survival rate of HUVECs was determined by tetrazolium assay.The intracellular activities of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),total nitric oxide synthase(NOS) and extracellular nitric oxide(NO) level were detected.The intracellular reactive oxygen species(ROS) level and the apoptotic index and cell cycle alteration were detected by flow cytometry.Results Geniposide concentration-dependently increased the viability of injured endotheial cells,while increased the activity of SOD,GSH-Px,NOS and NO production.The intracellular ROS level and the apoptotic index were reduced by geniposide.The cell proliferation was increased with geniposide incubation.Conclusion Geniposid may be a potential anti-oxidation agent which has a protective effect against HUVEC injuries induced by H2O2.

Colleges are important places which cultivate high-tech talent and implement tech-nological innovation. In the management mechanism, the experimental teaching center, a secondary teaching unit of Chongqing Medical University, can integrates teaching resources effectively. Accord-ing to experimental teaching program , the hierarchical experimental teaching curriculum reform has been carried out. By performing open and innovative experiment of medical practice, standardizing the practice process of innovative experiment project, improving the activity of students to participate in the project, we try to explore the new way of medical talent cultivation.

Objective To investigate the applicafion value of a simple stereotaxic technology in open biopsy of breast calcification with wire localization guided by X-ray.Methods 36 lesions in 30 cases with calcifications on mammography underwent X-ray guided simple wire stereotaxic localization open biopsy.Results 36 lesions in 30 cases were removed completely after wire localization,among which 24 cases were removed completely by one time,accounting for 80％ (24/30)of the total,and 6 cases were removed completely by two times,accounting for 20％ (6/30)of the total.No case were removed without calcification or removed completely by more than three times.Conclusion The simple stereotaxic technology in open biopsy of breast calcification with wire localization guided by X-ray is easy to learn and safe to do,which is suitable for promotion at the grassroots hospital.

Objective To investigate the mechanisms that mediate the neuroprotective effect of the intestinal microbial metabolite sodium butyrate(NaB)in a mouse model of Parkinson's disease(PD)via the gut-brain axis.Methods Thirty-nine 7-week-old male C57BL/6J mice were randomized equally into control group,PD model group,and NaB treatment group.In the latter two groups,PD models were established by intraperitoneal injection of 30 mg/kg 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)once daily for 5 consecutive days,and normal saline was injected in the control group.After modeling,the mice received daily gavage of NaB(300 mg/kg)or an equal volume of saline for 14 days.Behavioral tests were carried out to assess the changes in motor function of the mice,and Western blotting was performed to detect the expressions of tyrosine hydroxylase(TH)and α-synuclein(α-syn)in the striatum and nuclear factor-κB(NF-κB),tumor necrosis factor(TNF-α),interleukin 6(IL-6),and the tight junction proteins ZO-1,Occludin,and Claudinin the colon.HE staining was used to observe inflammatory cell infiltration in the colon of the mice.RNA sequencing analysis was performed to identify the differentially expressed genes in mouse colon tissues,and their expressions were verified using qRT-PCR and Western blotting.Results The mouse models of PD with NaB treatment showed significantly increased movement speed and pulling strength of the limbs with obviously upregulated expressions of TH,Occludin,and Claudin and downregulated expressions of α-syn,NF-κB,TNF-α,and IL-6(all P<0.05).HE staining showed that NaB treatment significantly ameliorated inflammatory cell infiltration in the colon of the PD mice.RNA sequencing suggested that Bmal1 gene probably mediated the neuroprotective effect of NaB in PD mice(P<0.05).Conclusion NaB can improve motor dysfunction,reduce dopaminergic neuron loss in the striatum,and ameliorate colonic inflammation in PD mice possibly through a mechanism involving Bmal1.

Objective To investigate the mechanisms that mediate the neuroprotective effect of the intestinal microbial metabolite sodium butyrate(NaB)in a mouse model of Parkinson's disease(PD)via the gut-brain axis.Methods Thirty-nine 7-week-old male C57BL/6J mice were randomized equally into control group,PD model group,and NaB treatment group.In the latter two groups,PD models were established by intraperitoneal injection of 30 mg/kg 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)once daily for 5 consecutive days,and normal saline was injected in the control group.After modeling,the mice received daily gavage of NaB(300 mg/kg)or an equal volume of saline for 14 days.Behavioral tests were carried out to assess the changes in motor function of the mice,and Western blotting was performed to detect the expressions of tyrosine hydroxylase(TH)and α-synuclein(α-syn)in the striatum and nuclear factor-κB(NF-κB),tumor necrosis factor(TNF-α),interleukin 6(IL-6),and the tight junction proteins ZO-1,Occludin,and Claudinin the colon.HE staining was used to observe inflammatory cell infiltration in the colon of the mice.RNA sequencing analysis was performed to identify the differentially expressed genes in mouse colon tissues,and their expressions were verified using qRT-PCR and Western blotting.Results The mouse models of PD with NaB treatment showed significantly increased movement speed and pulling strength of the limbs with obviously upregulated expressions of TH,Occludin,and Claudin and downregulated expressions of α-syn,NF-κB,TNF-α,and IL-6(all P<0.05).HE staining showed that NaB treatment significantly ameliorated inflammatory cell infiltration in the colon of the PD mice.RNA sequencing suggested that Bmal1 gene probably mediated the neuroprotective effect of NaB in PD mice(P<0.05).Conclusion NaB can improve motor dysfunction,reduce dopaminergic neuron loss in the striatum,and ameliorate colonic inflammation in PD mice possibly through a mechanism involving Bmal1.