ABSTRACT
Objective:To observe the effect of exogenous hydrogen sulfide(H 2S) on the proliferation of rabbit vascular smooth muscle cell(VSMC) under high static pressure. Methods:Rabbit thoracic aorta VSMC were isolated and cultured under high static pressure(100mmHg) and divided into control group [cultured with 0.2%fetal bovine serum(FBS) and no NaHS]、10%FBS group(10%FBS and no NaHS) and NaHS group(10%FBS and 50mmol/L NaHS). VSMC proliferation was analyzed with BUDR. CSE, Calmodulin(p-CaM)and CyclinD1 protein levels of VSMC were measured by Western blotting.Results:Compared with the 10%FBS group, NaHS inhibit the proliferation of rabbit VSMC significantly (0.50±0.03 vs. 0.26±0.03, P<0.05). Compared with control group, CSE protein in the 10%FBS group decreased significantly(1.21±0.10 vs. 0.33±0.04, P<0.05) and p-CaM and CyclinD1 protein increased significantly(0.23±0.04 vs. 0.86±0.04 and 0.22±0.03 vs. 1.19±0.06, P<0.05). Compared with the 10%FBS group, CSE protein in NaHS group increased significantly(0.33±0.04 vs. 1.11±0.11, P<0.05), and the expression of p-CaM and CyclinD1 protein decreased significantly(0.86±0.04 vs. 0.26±0.05 and 1.19±0.06 vs. 0.51±0.03, P<0.05). Conclusion:Exogenous hydrogen sulfide inhibits the proliferation of VSMC under high static pressure by the CSE/H2S pathway which related to the reduction of the expression of p-CaM and CyclinD1.
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Objective To observe the effect of GLP-1 on HSP70 expression of rabbit thoracic aortic endothelial cells at high glucose level.Methods Rabbit thoracic aortic endothelial cells were isolated and cultured.Tunnel was used to assay endothelial cells apoptosis.Cell proliferation was analyzed with BUDR.The protein level of HSP70 were detected by Western blot.Results The proliferation of rabbit thoracic aortic endothelial cells cultured under high glucose (33 mmol/L) decreased,(0.54 ±0.06 vs 0.78 ±0.04,P ＜ 0.01).The apoptosis and the protein level of HSP70 increased,(36.43％ ± 6.85％ vs 5.25％ ±0.73％) and (0.94 ± 0.11 vs 0.29 ± 0.03,all P ＜ 0.01).The proliferation of rabbit thoracic aortic endothelial cells (0.62 ± 0.06)in the GLP-1 group increased,the apoptosis ratio (10.13％ ± 1.19％) and HSP70 expression (0.76 ± 0.05) decreased significantly (P ＜ 0.05) compared with high glucose group.Conclusion GLP-1 can ameliorate high-glucose-induced rabbit thoracic aortic endothelial cells apoptosis and promote cell proliferation,attenuating high-glucose-induced level of HSP70 expression through the GLP-1 R-dependent pathways.
ABSTRACT
Objective To explore the clinical significance of retrograde access for the interventional treatment of lower extremity arterial occlusive diseases when the occluded segment of lower extremity artery could not be reached through antegrade access.Methods Twenty-seven cases (male 17,female 10; age range 32-89 years ) were retrospectively investigated, including 18 with lower limb arteriosclerosis obliterans,7 with diabetic foot and 2 with thromboangiitis obliterans.According to the Fontaine staging,6 cases were classified as Fontaine Ⅱ,11were classified as Fontaine Ⅲ and 10 were classified as Fontaine Ⅳ.All cases underwent endovascular operation through antegrade access first with an attempt to cross the occlusive segment,but in vain.So retrograde access was tried via puncture of pedis dorsalis or posterior tibial artery or exposure of lateral branches of posterior tibial artery,peroneal artery or dorsal artery by open surgery,which followed by Percutaneous transluminal angiography and (or) stenting.Results The operation through retrograde access was successful in all cases with obvious improvement of ischemic symptoms.Hematoma at the puncture site occurred in 3 patients,and paresthesia of toes occurred in 1after dorsalis pedis arteriotomy.No severe perioperative complication occurred.The average ankle brachial index increased from 0.37 ± 0.11preoperatively to 0.85 ± 0.12 postoperatively.Conclusions Retrograde access could be used as an alternative strategy in lower extremity arterial occlusive diseases when the occluded segment could not reach through antegrade access.