AIM:To explore the effect of microRNA-296-5p(miR-296-5p)on neurological damage after cere-bral infarction(CI)and its regulatory relationship with angiotensin-converting enzyme 2(ACE2)signaling pathway medi-ated proliferation of endothelial progenitor cell(EPC).METHODS:Serum samples from 70 patients diagnosed with CI and accompanied by neurological damage in our hospital(CI group)and 70 healthy volunteers(healthy group)were se-lected.The mRNA expression of miR-296-5p,ACE2,and Mas in the serum of both groups were detected by RT-qPCR.The rat model of CI was constructed and SD rats were randomly divided into healthy control group,model control group,sh-miR-296-5p group,and ACE2 overexpression group(OE-ACE2 group).Neurological severity scores(NSS)score was evaluated.The CI status of rats in each group was observed by TTC staining.The mRNA expression of miR-296-5p,ACE2,and Mas in serum of rat was detected by RT-qPCR.EPC were isolated and cultured routinely,and were randomly divided into control group,sh-miR-296-5p group,OE-ACE2 group,OE-miR-296-5p+OE-ACE2 group,and sh-miR-296-5p+sh-ACE2 group.The viability of EPC was detected by CCK-8.Apoptosis of EPC was detected by flow cytometry.The mRNA expression of miR-296-5p,ACE2,and Mas in EPC was detected by RT-qPCR.The relationship between miR-296-5p and ACE2 was verified by dual luciferase reporter gene assay.RESULTS:(1)Clinical trial:compared with the healthy group,the level of miR-296-5p in serum of CI patients was obviously increased(P<0.05),while the mRNA ex-pression levels of ACE2 and Mas were obviously reduced(P<0.05).(2)Animal experiments:compared with the healthy control group,the NSS score,CI area,the level of miR-296-5p in serum,and the mRNA expression level of Mas in the model control group were obviously increased(P<0.05),while the mRNA expression level of ACE2 was obviously de-creased(P<0.05).Compared with the model control group,the NSS score,CI area,the level of miR-296-5p in serum,and the mRNA expression level of Mas in the sh-miR-296-5p group and OE-ACE2 group were obviously reduced(P<0.05),while the mRNA expression level of the ACE2 was obviously increased(P<0.05).(3)Cell experiment:Com-pared with the control group,the A450 and the level of miR-296-5p of EPC cells in the sh-miR-296-5p group and OE-ACE2 group were obviously reduced(P<0.05),the apoptosis rate,the mRNA expression level of ACE2,and Mas were obvious-ly increased(P<0.05).Compared with the sh-miR-296-5p group,the A450 and the level of miR-296-5p in the sh-miR-296-5p+sh-ACE2 group were obviously increased(P<0.05),the apoptosis rate,the mRNA expression level of ACE2,and Mas were obviously reduced(P<0.05).Compared with the OE-ACE2 group,the level of A450 and miR-296-5p in OE-miR-296-5p+OE-ACE2 group were obviously increased(P<0.05),the apoptosis rate,the mRNA expression level of ACE2,and Mas were obviously reduced(P<0.05).CONCLUSION:Knockdown of miR-296-5p may inhibit EPC proliferation by mediating the ACE2 signaling pathway,and alleviate neurological damage after CI.

Objective To compare intramedullary nailing assisted by minimally invasive cerclage with simple intramedullary nailing in the treatment of femoral long oblique subtrochanteric fractures.Methods From April 2010 to September 2015,our department treated 39 patients with femoral long oblique subtrochanteric fracture.Of them,16 were treated by cephalomedullary nailing combined with minimally invasive cerclage (observation group of 11 males and 5 females with an average age of 42.8 ± 13.2 years) and 23 by simple cephalomedullary nailing (control group of 17 males and 6 females with an average age of 46.2 ± 10.1 years).Their operation time,intraoperative blood loss,radiologic results (union time and alignment) and functional results [Visual Analog Scale (VAS) and Harris hip score] were compared between the 2 groups.Results The 39 patients were followed up from 12 to 30 months (average,15 months).For the observation group,the varus angle (2.2°± 1.4°) was significantly smaller than for the control group(4.1°±2.2°),the VAS scores at 1 and 3 months postoperatively (3.43 ± 1.54,1.13 ± 1.20) were significantly lower than for the control group (5.61 ± 1.41,3.34 ± 1.82),and the clinical union ratio at 3 months postoperatively(87.5％,14/16) significantly higher than for the control group (47.8％,11/23) (P ＜ 0.05).There were no significant differences between the 2 groups in terms of operation time,intraoperative blood loss,Harris hip score at one year postoperatively,VAS score at 6 months postoperatively,or clinical union ratio at 6 or 12 months postoperatively(P ＞ 0.05).Conclusions Cephalomedullary nailing is effective for the treatment of femoral long oblique subtrochanteric fractures no matter it is assisted by minimally invasive cerclage or not.However,since minimally invasive cerclage has the advantage of improving reduction and mechanical stability,combination of minimally invasive cerclage and cephalomedullary nailing may be more advantageous in early pain-relieving and functional recovery.

Objective To evaluate the effects of andrographolide on insulin resistance,dysbiosis and Notch/zinc finger protein transcription factor 1(Snail1)signaling pathway in diabetic rats.Methods A total of 70 male Wistar rats with SPF grade were selected,and 30 of them were selected for andrographolide LD50 test.After determining the lethal dose,50 mg/kg was selected for administration and observation,the remaining 40 rats,10 were used as the NC group,30 were established as the diabetes model,and a total of 28 rats were successfully modeled,which were divided into T2DM group(n=9),Metformin treatment group(Met,n=9),and andrographolide administration group(And,n=10).The NC group and T2DM group were not treated.The changes were evaluated after 14 days of intervention.Results Compared with NC group,HOMA-IR,the abundance levels of Bacteroidetes,Firmicute,mRNA and protein expression levels of Notch and Snail1,and positive expression rates were increased(P<0.05),while the abundance levels of Lactobacillus and Bifidobacterium were decreased in T2DM,Met and And group(P<0.05).Compared with T2DM group,HOMA-IR,the abundance levels of Bacteroidetes,Firmicute,mRNA and protein expression levels of Notch and Snail1,and positive expression rates were decreased,while the abundance levels of Lactobacillus and bifidobacterium were increased in Met and And group(P<0.05).Conclusions After andrographolide intervention,insulin resistance was alleviated,microbiota imbalance was improved,and Notch/Snail1 signaling pathway was suppressed in diabetic rats.

Objective To investigate the effect of atractylenolide Ⅲ(A Ⅲ)on stroke in spon-taneously hypertensive rats by regulating microRNA-296-5p(miR-296-5p)expression.Methods The spontaneously hypertensive rats(SHR)were given 0.9％sodium chloride solution freely for 2 months,and then fed with 1％sodium chloride solution to establish the stroke model of SHR.The rat models were randomly grouped into Model group,A Ⅲ low-dose group(A Ⅲ-L group),A Ⅲ high-dose group(A Ⅲ-H group),positive drug nimodipine group(Nim group),miR-296-5p agonist group(miR-296-5p agomir group),agomir NC group,A Ⅲ-H+miR-296-5p agomir group,and A Ⅲ-H+agomir NC group,with 12 in each group.The changes in neurological symptom scores,av-erage arterial pressure,survival time,and platelet adhesion rate were detected and recorded;hema-toxylin and eosin(HE)staining was applied to detect pathological changes in the CA1 region of the rat hippocampus;quantitative reverse transcription polymerase chain reaction(qRT-PCR)was ap-plied to detect the expression of miR-296-5p in the hippocampal CA1 region.Results Compared with the NC group,the Model group showed increases in neurological symptom score,mean arterial pressure,platelet adhesion rate,miR-296-5p expression,shortened survival time,and severe pathological damage to the hippocampal CA1 area(P＜0.05);compared with the Model group,the neurological symptom scores,mean arterial pressure,platelet adhesion rate,and miR-296-5p expression in the A Ⅲ-L,A Ⅲ-H,and Nim groups decreased,the survival time was prolonged,and the pathological damage in the CA1 area of the hippocampus was alleviated(P＜0.05);compared with Model group and agomir NC group,neurological symptom score,mean arterial pressure,platelet adhesion rate and miR-296-5p expression of rats in the miR-296-5p agomir group were increased,survival time was shortened,and pathological damage in hippocampal CA1 region was aggravated(P＜0.05).compared with the A Ⅲ-H group and the AⅢ-H+agomir NC group,the neurological symptom score,average arterial pressure,platelet adhesion rate and miR-296-5p expression of rats were in-creased,the survival time was shortened,and the pathological damage in hippocampal CA1 region was serious in the AⅢ-H+miR-296-5p agomir group(P＜0.05).Conclusion A Ⅲ may treat SHR stroke by inhibiting the expression of miR-296-5p.

Objective To investigate the effect of atractylenolide Ⅲ(A Ⅲ)on stroke in spon-taneously hypertensive rats by regulating microRNA-296-5p(miR-296-5p)expression.Methods The spontaneously hypertensive rats(SHR)were given 0.9％sodium chloride solution freely for 2 months,and then fed with 1％sodium chloride solution to establish the stroke model of SHR.The rat models were randomly grouped into Model group,A Ⅲ low-dose group(A Ⅲ-L group),A Ⅲ high-dose group(A Ⅲ-H group),positive drug nimodipine group(Nim group),miR-296-5p agonist group(miR-296-5p agomir group),agomir NC group,A Ⅲ-H+miR-296-5p agomir group,and A Ⅲ-H+agomir NC group,with 12 in each group.The changes in neurological symptom scores,av-erage arterial pressure,survival time,and platelet adhesion rate were detected and recorded;hema-toxylin and eosin(HE)staining was applied to detect pathological changes in the CA1 region of the rat hippocampus;quantitative reverse transcription polymerase chain reaction(qRT-PCR)was ap-plied to detect the expression of miR-296-5p in the hippocampal CA1 region.Results Compared with the NC group,the Model group showed increases in neurological symptom score,mean arterial pressure,platelet adhesion rate,miR-296-5p expression,shortened survival time,and severe pathological damage to the hippocampal CA1 area(P＜0.05);compared with the Model group,the neurological symptom scores,mean arterial pressure,platelet adhesion rate,and miR-296-5p expression in the A Ⅲ-L,A Ⅲ-H,and Nim groups decreased,the survival time was prolonged,and the pathological damage in the CA1 area of the hippocampus was alleviated(P＜0.05);compared with Model group and agomir NC group,neurological symptom score,mean arterial pressure,platelet adhesion rate and miR-296-5p expression of rats in the miR-296-5p agomir group were increased,survival time was shortened,and pathological damage in hippocampal CA1 region was aggravated(P＜0.05).compared with the A Ⅲ-H group and the AⅢ-H+agomir NC group,the neurological symptom score,average arterial pressure,platelet adhesion rate and miR-296-5p expression of rats were in-creased,the survival time was shortened,and the pathological damage in hippocampal CA1 region was serious in the AⅢ-H+miR-296-5p agomir group(P＜0.05).Conclusion A Ⅲ may treat SHR stroke by inhibiting the expression of miR-296-5p.