Aim To explore the effect of propofol preconditioning on myocardial ischemia/reperfusion injury and the role of phspho-ERK1/2 during the propofol preconditioning in renal hypertension rat(RHR).Methods The isolated RHR hearts perfused on langendorff apparatus were randomly divided into 8 groups(n=8 each).After 20 min of perfusion for equilibration,the CTRL group was subsequently perfused by 148 min.The ISCH group was submitted to 35 min of ischemia and 60 min of reperfusion(I/R) to induce ischemia/reperfusion injury.The DMSO group was given by once 18 min and twice 10 min K-H solution containing 20 ?mol?L~(-1) DMSO and 5 min K-H solution reperfusion prior to I/R procedure.The three propofol preconditioning groups were preconditioned by giving 2 cycles of 10 min K-H solution containing 30 ?mol?L~(-1),100 ?mol?L~(-1) or 300 ?mol?L~(-1) propofol and 5 min K-H solution reperfusion prior to the I/R procedure.The PD group and the PD+P100 group were given K-H solution containing 20 ?mol?L~(-1) PD98059,an ERK1/2 kinase specific inhibitor,for 18 min and 5 min K-H solution washout before I/R and 100 ?mol?L~(-1) PPC respectively.Cardiac functional indices were recorded.Activity of SOD and content of MDA were measured.The level of phspho-ERK1/2 protein expression was measured using Western Blotting.Results Compared with those in the CTRL group,the recovery of cardiac functional indices in ISCH group became worse(P

Animals ; Hindlimb ; blood supply ; Ischemic Preconditioning ; Lung ; metabolism ; Male ; P-Selectin ; metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism

Murine interleukin-4 gene(mIL-4) was transfected into mice glioblastoma cell line G422 by recombinant adenovirus vector. We detected mRNA transcription of target gene in gene modified tumor cells(G422-mIL4). High level of mouse IL-4 could be detected in the culture supernatant of G422-mIL4. When inoculated subcuatneously, the tumor growth of G422-mIL4 was significantly inhibited as compared to wild type G422 and LacZ gene modified G422( G422-LacZ) . The period of survival of mice inoculated with G422-mlL4 was significantly prolongated(p

Aim To investigate the inhibitory effect of schizandrin B( SchB) on ultraviolet radiation b ( UVB) radiation-induced apoptosis of HaCaT cells. Methods Methyl thiazolyl tetrazolium ( MTT ) assay was used to examine the effect of SchB on cell viability recovery. Cell apoptosis and necrosis were measured by Ho-chest33342 staining. The p53, p21 and Caspase-3 mRNA expressions were examined by RT-PCR. Results In this study, we found that Sch B attenuated UVB-in-duced toxicity in HaCaT cells. Through Hoechst 33342 stain, we visualized that SchB could inhibit UVB-in-duced HaCaT cell death. The result demonstrated that p53 , p21 and Caspase-3 mRNA levels decreased com-pared with the control group. Conclusions Sch B at-tenuates the UVB-induced toxicity of HaCaT by inhibi-ting apoptotic gene expression. It plays a role in anti-photoaging.

OBJECTIVE:To study the effects of podophyllotoxin derivative QW-83 on human cervical cancer HeLa cell apopto-sis and its mechanism. METHODS:After treated with 0(negative control),0.01,0.1,1 and 10 μmol/L QW-83 and positive drug etoposide(VP-16)for 48 h,proliferation inhibition rate and IC50 of HeLa cell were determined by MTT assay. The morphological changes of HeLa cell were observed by Hochest 33342 staining after treated with QW-83 [0(negative control),2.5,5,10μmol/L] for 48 h;flow cytometry was used to detect apoptosis rate;semi quantitative RT-PCR was adopted to detect the expression of apop-tosis related gene P53,Bax,Casepase-3,Casepase-8,Casepase-9 and Bcl-2 mRNA. RESULTS:Compared with negative control, 1,10 μmol/L VP-16 and QW-83 had obvious proliferation inhibition effect on HeLa cells (P<0.05 or P<0.01),and IC50 were (5.11±0.43)μmol/L and(4.96±0.54)μmol/L. Hochest 33342 staining results showed QW-83 could obviously induce cells apopto-sis and nuclear pyknosis. Flow cytometry showed QW-83 could increase apoptosis rate in concentration-dependent manner,being 16.89%-62.56%. RT-PCR showed mRNA expression of P53,Bax,Caspase-3,Casepase-8 and Casepase-9,Bcl-2/Bax increased, while mRNA expression of Bcl-2 decreased after treated with QW-83(P<0.05). CONCLUSIONS:Podophyllotoxin derivative QW-83 can induce HeLa cell apoptosis,and its mechanism may be associated with regulate mRNA expression of apoptosis related gene.

Objective To investigate the safety and effectiveness of using low-profile visualized intraluminal support (LVIS) stents for the treatment of aneurysms in the small intracranial vessels (diameter <2.5 mm).Methods Between October 2014 and April 2016,the clinical data of all 30 patients with intracranial saccular aneurysm treated with LVIS stents with the small parent arteries <2.5 mm in diameter in Changhai Hospital,the Second Military Medical University were analyzed retrospectively,including 7 ruptured aneurysms and 23 unruptured aneurysms.The anterior circulation aneurysm accounted for 93.3% (n=28),and the diameters of the parent arteries were 1.6-2.4 mm.The complications associated with surgery,angiography,clinical outcomes,and mid-term follow-up data were analyzed.Results The success rate of stent implantation was 100%.Immediate embolization results:Raymond grade Ⅰ in 12 cases (40.0%),Raymond grade Ⅱ in 11 cases (36.7%),and Raymond grade Ⅲ in 7 cases (23.3%).Complications occurred in 2 cases,including one perforating artery occlusion and one intraoperative rupture.Twenty-five patients accepted the angiographic follow-up (Raymond grade Ⅰ in 21 cases,grade Ⅱ in 3 cases,and grade Ⅲ in 1 case).The follow-up time ranged from 4 to 14 months,with an average of 8.1± 2.6 months.One patient had asymptomatic intracranial artery stenosis in the distal end of the stent.No new neurological dysfunction or death occurred.Conclusion The deployment of LVIS stents in small vessels is safe and feasible,the effect of mid-term follow-up is better.However,a larger sample study and long-term follow-up results are needed.

This study is to investigate the antitumor activity of CIP-36 on multidrug resistant human oral squamous carcinoma cell line (KBV200 cells) in vitro and the possible anticancer mechanisms. MTT assay, Hoechst fluorescein stain, RT-PCR and immunohistochemistry were carried out on KBV200 and KB cells. The growth of many tumor cells was obviously inhibited by CIP-36, especially the multidrug resistant cells KBV200. Obvious apoptosis could be observed in the Hoechst 33342 staining experiments. The results of RT-PCR showed that the levels of p53, p21, caspase-3 and bax mRNA increased, and meanwhile the expression of mdr-1 and bcl-2 mRNA decreased in a dose-dependent manner. The data were significantly different from that of vehicle. The expression of P-gp significantly decreased with the increasing dosage of CIP-36 examined by immunohistochemistry. It can be concluded that CIP-36 could change resistance-related genes and proteins to overcome multidrug resistance in the KBV200 cell line.

Structural modifications were performed with natural product of oleanolic acid to search for novel anticancer drugs. Ten oleanolic acid derivatives were designed and obtained by the reaction of oxidation, acylation or hydrolyzation, etc. The cytotoxic activity of derivatives was evaluated against HeLa, HepG2 and BGC-823 cells in vitro by MTT assay, gefitinib and etoposide used as a positive control. The results showed that compound 5a was particularly active to inhibit HepG2 cells growth, and anti-tumor activity of compound 7 on HeLa cells was significantly stronger than oleanolic acid. They are worthy to be studied further.

Objective To explore the protective effect of schisandrin B (SchB) on the permanent damage of human keratinocytes (HaCat) induced by long wave ultraviolet (UVA),and its possible mechanism thereof. Methods After HaCat was treated by 5 J/cm2 UVA, different concentrations of SchB (0.1, 0.01, 0.001 and 0.000 1μmol/L) were used to treat HaCat cells. The levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activity, lactate dehydrogenase (LDH) and NO content were detected. Results The levels of SOD and GSH-Px activity were decreased, and he levels of LDH and NO content were increased in HaCat cells after being treated by UVA. The different concentrations of SchB showed significant ef-fects on the increased levels of SOD, GSH-Px activity and decreased levels of LDH and NO, and improved the survival rate of HaCat cells. The 0.001 μmol/L SchB showed the strongest protective effect. Conclusion The 0.001 μmol/L SchB showed the best effect on the damage of HaCat cells induce the UVA.

Aim To study the mechanism of action of the new derivative of podophyllotoxin(LN-13)in indu-cing the apoptosis of K562/A02 cells.Methods The MTT method was taken to detect the inhibition of LN-13 and VP-16 on K562/A02 proliferation and inhibi-tion rate and IC50 values were obtained 48 hours later. The K562/A02 cell morphological change induced by LN-13 were observed through Hochest33342 and PI staining after 48 hours later.Flow cytometry was taken to detect the apoptosis of K562/A02 cells induced by LN-13.The reverse transcription-polymerase chain re-action was taken to detect the Bcl-2,Bax,caspase-3 and mdr-1 mRNA expression.The expression of P-gp was detected by Western blot.Results The growth of K562 /A02 cells was obviously inhibited by LN-13 when IC50 value was 3.32 μmol · L-1 .LN-13 could obviously induced cell apoptosis observed by Ho-chest33342 and PI staining.Flow cytometry detection showed that LN-13(2,4,8 μmol·L-1 )could induce cell apoptosis and apoptosis ratio reached 15.0%, 48.0%,68.96%,respectively.The reverse transcrip-tion-polymerase chain reaction showed that LN-13 in-creased the Bax and Caspase-3 mRNA expression,and meanwhile the expression of mdr-1 mRNA decreased. Western blot showed that P-gp expression was de-creased as the LN-13 dose increased.The data were significantly different from those of control group.Con-clusion Podophyllotoxin derivative LN-13 can induce the apoptosis of K562 /A02 cells,which may be close-ly-related to regulating P-gp expression and apoptosis related gene mRNA expression.