Expression Patterns of Sarcomeric α-Actin, α-Actinin and UCP_2 in the Myocardium of Kunming Mice after Exposure to C-Terminal Polypeptide of Cardiotrophin-1

Cardiotrophin-1 （CT-1） activates a distinct form of cardiac muscle cell hypertrophy in which the sarcomeric units are assembled in series. The aim of the study was to determine the expres- sion pattern of sarcomeric contractile protein α-actin, specialized eytoskeletal protein α-actinin and mitochondrial uncoupling protein-2 （UCP2） in myocardial remodeling induced by chronic exposure to CT-1. Kunming mice were intraperitoneally injected with carboxy-terminal polypeptide （CP） of CT-1 （CT-1-CP, 500 μg·kg-1·day^-1） for 1, 2, 3 and 4 week （s）, respectively （4 groups obtained according to the injection time, n=10 each, with 5 males and 5 females in each group）, Those injected with physiological saline for 4 weeks served as controls （n=10, with 5 males and 5 females）. The heart tissues of mice were harvested at 1, 2, 3 or 4 week （s）. Immunohistochemistry （IHC） and Western blotting （WB） were used to detect the distribution and expression of sarcomeric α-actin, α-aetinin and mitoehondrial UCP2 in myocardial tissues. IHC showed that α-actin was mainly distributed around the nuclei of cardiomyo- cytes, α-actinin concentrated around the striae and UCP2 scattered rather evenly in the plasma. The ex- pression of α-actin was slightly greater than that of α-actinin and UCP2 in the control group （IHC： χ^2=6.125; WB： F=0.249, P〉0.05） and it gradually decreased after exposure to CT-1-CP. There was no significant difference in the expression of α-actin between the control group and the CT-1-CP-treated groups （χ^2=7.386, P〉0.05）. But Western blotting revealed significant difference in the expression of α-actin between the control group and the 4-week CT-1-CP-treated group （F=2.912; q=4.203, P〈0.05）. Moreover, it was found that the expression of α-actinin increased stepwise with the exposure time in CT-1-CP-treated groups and differed significantly between CT-1-CP-treated groups and the control group （ICH： χ^2=21.977; WB： F=50.388; P〈0.01）. The expression of UCP2 was initially increased （WB： control group vs. 1- or 2-week group, q values： 5.603 and 9.995, respectively, P〈0.01） and then de- creased （WB： control group vs. 3-week group, q=4.742, P〈0.01; control group vs. 4-week group, q=0.558, P〉0.05）. It was suggested that long-term exposure to CT-1-CP could lead to the alteration in the expression of sarcomeric α-actin, α-actinin and mitochonclrial UCP2. The different expressions of sarcomeric structure proteins and mitochondrial UCP2 may be involved in myocardial remodeling.

AFAP-1L2通过PI3K/Akt通路影响胰腺癌细胞增殖及凋亡

目的:检测肌动蛋白丝相关蛋白1相似蛋白(actin filament-associated protein 1-like 2,A FA P-1L2)在不同分化程度胰腺癌细胞株中的表达,并观察其对下游磷脂酰肌醇3激酶/蛋白激酶(phosphatidylinositol 3 kinase/protein kinase B,PI3K/Akt)通路调控作用及对胰腺癌细胞的增殖、周期及凋亡的影响.方法:以Western blot及实时定量PCR检测(real-time quantitative PCR,q RT-PCR)法对不同分化程度胰腺癌细胞系PANC-1、Mia Pa Ca-2、Colo-357、BXPC-3、SW1990及CFPAC-1中AFAP-1L2表达进行检测;构建靶向AFAP-1L2的干扰质粒si AFAP-1L2,转染Mia Pa Ca-2细胞,以Western blot及q RTPCR法检测AFAP-1L2下调后PI3K/Akt通路蛋白及m RNA变化;四甲基偶氮唑盐微量酶反应比色法(methyl-thiazolyl-tetrazolium,MTT)法检测转染后Mia Pa Ca-2细胞增殖;流式细胞术检测细胞周期及凋亡.结果:Western blot及q RT-PCR法显示,AFAP-1L2蛋白及m R N A表达水平在低分化胰腺癌细胞系中表达水平高于中分化及高分化细胞系.si AFAP-1L2转染后磷脂酰肌醇3激酶a亚单位(P I3K C A)蛋白在s i A FA P-1L2组的表达量明显低于A FA P-1L2组及小干扰RNA(small interfering RNA,si RNA)control组(F=9.280,P=0.0139),a蛋白激酶(a-Akt)在si AFAP-1L2细胞的表达量高于MOCK细胞及si RNA control细胞(F=7.719,P=0.0219),磷酸化a蛋白激酶(a-p A k t)在si AFAP-1L2细胞的表达量低于MOCK细胞及si RNA control细胞(F=5.507,P=0.0439).PI3KCAm RNA在si AFAP-1L2组的表达量明显低于AFAP-1L2组及si RNA control组(F=20.16,P=0.0022),a-Akt m RNA在si AFAP-1L2细胞的表达量高于MOCK细胞及siRNA control细胞(F=6.068,P=0.0362),a-p Akt m R N A在s i A FA P-1L2细胞的表达量低于MOCK细胞及si RNA control细胞(F=10.33,P=0.0114).MTT检测显示,在48、72及96h siAFAP-1L2干扰后Mia PaCa-2细胞增殖能力下降(F=3.924,P<0.05;F=6.812,P<0.01;F=7.003,P<0.01).流式细胞检测显示,si AFAP-1L2干扰后G1期细胞比例增高,G2及S期比例减少(F=4.87,F=5.26,F=4.94,均P<0.05),si AFAP-1L2干扰后Mia Pa Ca-2细胞凋亡率增高(F=7.231,P<0.01).结论:在分化程度低的胰腺癌细胞中AFAP-1L2表达较高,AFAP-1L2通过PI3K/Akt通路影响胰腺癌细胞增殖、细胞周期及凋亡,可作为胰腺癌治疗新的靶向候选基因.

CircACTR2调节miR-23a-3p/TBL1X轴对高糖诱导的滋养层细胞损伤的影响

目的探讨环状RNA肌动蛋白相关蛋白2(circACTR2)调节miR-23a-3p/转导素β1X连锁蛋白(TBL1X)轴对高糖诱导的滋养层细胞损伤的影响。方法将人绒毛膜滋养层细胞HTR-8/Svneo分为NG组(5.5 mmol/L葡萄糖)、HG组(25 mmol/L葡萄糖)、si-NC组(25 mmol/L葡萄糖+转染si-NC)、si-circACTR2组(25 mmol/L葡萄糖+转染si-circACTR2)、si-circACTR2+inhibitor-NC组(25 mmol/L葡萄糖+si-circACTR2和inhibitor-NC共转染)、sicircACTR2+miR-23a-3p inhibitor组(25 mmol/L葡萄糖+si-circACTR2和miR-23a-3p inhibitor共转染)。实时荧光定量PCR(qPCR)检测细胞中circACTR2、miR-23a-3p的表达;CCK-8法检测细胞增殖;流式细胞仪检测细胞凋亡;划痕实验检测细胞迁移;酶联免疫吸附试验检测丙二醛(MDA)水平和乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)活性;Western blot检测细胞中TBL1X、增殖细胞核抗原(PCNA)、基质金属蛋白酶(MMP)-2、MMP-9、胱天蛋白酶3(caspase-3)的表达。双萤光素酶报告基因实验分别验证circACTR2、TBL1X和miR-23a-3p的靶向关系。结果与NG组相比,HG组HTR-8/Svneo细胞miR-23a-3p表达、增殖能力、划痕愈合率、PCNA、MMP-2、MMP-9表达、SOD活性降低,circACTR2、TBL1X和caxpase-3表达、MDA含量、LDH活性、凋亡率升高(P<0.05);与HG组和si-NC组相比,si-circACTR2组HTR-8/Svneo细胞中miR-23a-3p表达、增殖能力、划痕愈合率、PCNA、MMP-2、MMP-9表达、SOD活性升高,circACTR2、TBL1X和caxpase-3表达、MDA含量、LDH活性、凋亡率降低(P<0.05);在敲低circACTR2的基础上,下调miR-23a-3p可明显减弱circACTR2敲低对高糖诱导的HTR-8/Svneo细胞的增殖和迁移的促进作用,增强细胞凋亡和氧化应激能力。双萤光素酶报告基因实验结果显示,circACTR2靶向负调控miR-23a-3p表达,miR-23a-3p靶向负调控TBL1X表达。结论敲低circACTR2可调控miR-23a-3p/TBL1X轴,进而通过抑制高糖诱导的滋养层细胞损伤来发挥保护作用。

Evaluation of trabecular meshwork-specific promoters in vitro and in vivo using scAAV2 vectors expressing C3 transferase

AIM:To evaluate the potential of two trabecular meshwork(TM)-specific promoters,Chitinase 3-like 1(Ch3L1)and matrix gla protein(MGP),for improving specificity and safety in glaucoma gene therapy based on self-complementary AAV2(scAAV2)vector technologies.METHODS:An scAAV2 vector with C3 transferase(C3)as the reporter gene(scAAV2-C3)was selected.The scAAV2-C3 vectors were driven by Ch3L1(scAAV2-Ch3L1-C3),MGP(scAAV2-MGP-C3),enhanced MGP(scAAV2-eMGP-C3)and cytomegalovirus(scAAV2-CMV-C3),respectively.The cultured primary human TM cells were treated with each vector at different multiplicities of infections.Changes in cell morphology were observed by phase contrast microscopy.Actin stress fibers and Rho GTPases/Rho-associated protein kinase pathway-related molecules were assessed by immunofluorescence staining,real-time quantitative polymerase chain reaction and Western blot.Each vector was injected intracamerally into the one eye of each rat at low and high doses respectively.In vivo green fluorescence was visualized by a Micron III Retinal Imaging Microscope.Intraocular pressure(IOP)was monitored using a rebound tonometer.Ocular responses were evaluated by slit-lamp microscopy.Ocular histopathology analysis was examined by hematoxylin and eosin staining.RESULTS:In TM cell culture studies,the vectormediated C3 expression induced morphologic changes,disruption of actin cytoskeleton and reduction of fibronectin expression in TM cells by inhibiting the Rho GTPases/Rhoassociated protein kinase signaling pathway.At the same dose,these changes were significant in TM cells treated with scAAV2-CMV-C3 or scAAV2-Ch3L1-C3,but not in cells treated with scAAV2-eMGP-C3 or scAAV2-MGP-C3.At lowinjected dose,the IOP was significantly decreased in the scAAV2-Ch3L1-C3-injected eyes but not in scAAV2-MGPC3-injected and scAAV2-eMGP-C3-injected eyes.At highinjected dose,significant IOP reduction was observed in the scAAV2-eMGP-C3-injected eyes but not in scAAV2-MGP-C3-injected eyes.Similar to scAAV2-CMV-C3,scAAV2-Ch3L1-C3 vector showed efficient transduction both in the TM and corneal endothelium.In anterior segment tissues of scAAV2-eMGP-C3-injected eyes,no obvious morphological changes were found except for the TM.Inflammation was absent.CONCLUSION:In scAAV2-transduced TM cells,the promoter-driven efficiency of Ch3L1 is close to that of cytomegalovirus,but obviously higher than that of MGP.In the anterior chamber of rat eye,the transgene expression pattern of scAAV2 vector is presumably affected by MGP promoter,but not by Ch3L1 promoter.These findings would provide a useful reference for improvement of specificity and safety in glaucoma gene therapy using scAAV2 vector.

Prognostic value of the long noncoding RNA AFAP1-AS1 in cancers

Objective This meta-analysis explored whether the expression of actin filament-associated protein 1 antisense RNA 1(AFAP1-AS1)is related to the prognosis and clinicopathological features of patients with cancer.Methods PubMed,EMBASE,and Cochrane Library were systematically searched.Hazard ratios(HRs)with 95%confidence intervals(CIs)were used to assess the prognostic value based on overall survival(OS),disease-free survival(DFS),and progression-free survival(PFS).Odds ratios(ORs)with 95%CIs were used to determine the relationships between AFAP1-AS1 and clinicopathological features,such as large tumor size(LTS),high tumor stage(HTS),poor histological grade(PHG),lymph node metastasis(LNM),and distant metastasis(DM).Results Thirty-five eligible articles and 3433 cases were analyzed.High AFAP1-AS1 expression,compared to low AFAP1-AS1 expression,correlated with significantly shorter OS(HR=2.15,95%CI=1.97-2.34,P<0.001),DFS(HR=1.37,95%CI=1.19-1.57,P<0.001),and PFS(HR=1.97,95%CI=1.56-2.50,P<0.001)in patients with cancer.In various cancers,elevated AFAP1-AS1 expression was significantly associated with LTS(OR=2.76,95%CI=2.16-3.53,P<0.001),HTS(OR=2.23,95%CI=1.83-2.71,P<0.001),and PHG(OR=1.39,95%CI=1.08-1.79,P=0.01)but not LNM(OR=1.59,95%CI=0.88-2.85,P=0.12)or DM(OR=1.81,95%CI=0.90-3.66,P=0.10).Conclusion High AFAP1-AS1 expression was associated with prognostic and clinicopathological features,suggesting that AFAP1-AS1 is a prognostic biomarker for human cancers.

AFAP-1L2对胰腺癌细胞侵袭及转移的影响及机制

目的:探讨AFAP-1L2表达下调对胰腺癌细胞的影响及其机制。方法:人胰腺癌SW1990细胞分别转染靶向AFAP-1L2的干扰质粒si AFAP-1L2和阴性对照si RNA,以未处理的SW1990细胞为空白对照,检测各组细胞的迁移与侵袭能力,以及肿瘤浸润相关分子的蛋白与m RNA变化;免疫共沉淀法检测AFAP-1L2蛋白与p85α蛋白相互作用关系。结果:与空白对照SW1990细胞比较,转染si AFAP-1L2下调AFAP-1L2后,SW1990细胞的迁移与侵袭能力明显降低,p85α及α-p Akt表达降低,α-Akt表达升高(均P<0.05),MMP-9与E-cadherin表达无变化(均P>0.05);转染阴性对照si RNA的SW1990细胞各项指标无明显变化(均P>0.05)。免疫共沉淀显示,胰腺癌SW1990细胞中AFAP-1L2蛋白与p85α蛋白存在相互作用。结论:AFAP-1L2可能通过与p85α相互作用调控PI3K/Akt通路,从而影响胰腺癌细胞的迁移及浸润,下调AFAP-1L2表达能抑制胰腺癌细胞迁移与侵袭能力。

下调XB130表达对胃癌HGC-27细胞增殖及凋亡的影响

【目的】观察下调肌动蛋白丝相关蛋白1相似蛋白2(actin filament-associated protein 1-like 2,XB130)表达对胃癌细胞增殖及凋亡的影响并探讨其机制。【方法】以Western blotting及q RT-PCR检测4种胃癌细胞株(HGC-27、KATOⅢ、N87、SNU-1)中XB130表达水平;构建小RNA干扰质粒si XB130,转染HGC-27细胞,以Western blotting及q RT-PCR检测转染效率及转染后凋亡相关基因(Cleaved-PARP、Cleaved-Caspase3)表达水平;MTT法检测转染后细胞增殖,流式细胞术检测转染后细胞凋亡。【结果】4种胃癌细胞株中XB130蛋白及m RNA均有表达,其中以HGC-27细胞表达水平最高。转染si XB130至HGC-27细胞后显示,si XB130组细胞增殖率在72 h及96 h低于MOCK组及si NC组(F=3.991,P<0.05;F=2.804,P<0.05),而凋亡率则高于MOCK组及si NC组(F=14.261,P<0.001);与MOCK及si NC组对比,si XB130组中Cleaved-PARP蛋白及m RNA表达水平降低,CleavedCaspase3则升高。【结论】下调胃癌细胞XB130表达可抑制增殖和促进其凋亡,XB130可作为胃癌治疗靶向候选基因。

LncRNA AFAP1-AS1/miR-27b-3p/VEGF-C axis modulates stemness characteristics in cervical cancer cells

Background:Long non-coding RNA(lncRNA)actin filament-associated protein 1 antisense RNA 1(AFAP1-AS1)functions as a competing endogenous RNA to regulate target genes expression by sponging microRNAs(miRs)to play cancer-promoting roles in cancer stem cells.However,the regulatory mechanism of AFAP1-AS1 in cervical cancer(CC)stem cells is unknown.The present study aimed to provide a new therapeutic target for the clinical treatment of CC.Methods:Hyaluronic acid receptor cluster of differentiation 44 variant exon 6(CD44v6)(+)CC cells were isolated by flow cytometry(FCM).Small interfering RNAs of AFAP1-AS1(siAFAP1-AS1)were transfected into the(CD44v6)(+)cells.The levels of AFAP1-AS1 were measured by quantitative real-time PCR(qRT-PCR).Sphere formation assay,cell cycle analysis,and Western blotting were used to detect the effect of siAFAP1-AS1.RNA pull-down and luciferase reporter assay were used to verify the relationship between miR-27b-3p and AFAP1-AS1 or vascular endothelial growth factor(VEGF)-C.Results:CD44v6(+)CCcells had remarkable stemness and a high level ofAFAP1-AS1.However,AFAP1-AS1knockdownwithsiAFAP1-AS1suppressed the cell cycle transitionofG(1)/S phase and inhibited self-renewal ofCD44v6(+)CCcells,the levels of the stemnessmarkers octamer-binding transcription factor 4(OCT4),osteopontin(OPN),and cluster of differentiation 133(CD133),and the epithelialmesenchymal transition(EMT)-related proteins Twist1,matrix metalloprotease(MMP)-9,and VEGF-C.In the mechanism study,miR-27b-3p/VEGF-C signaling was demonstrated to be a key downstream of AFAP1-AS1 in the CD44v6(+)CC cells.Conclusions:LncRNA AFAP1-AS1 knockdown inhibits the CC cell stemness by upregulating miR-27b-3p to suppress VEGF-C.

CRISPR-Cas9-based genome-wide screening identified novel targets for treating sorafenib-resistant hepatocellular carcinoma:a cross-talk between FGF21 and the NRF2 pathway

The treatment of hepatocellular carcinoma(HCC)has been dominated by multikinase inhibitors for more than a decade.However,drug resistance can severely restrict the efficacy of these drugs.Using CRISPR/CAS9 genome library screening,we evaluated Kelch-like ECH-associated protein 1(KEAP1)as a key regulator of sorafenib’s susceptibility in HCC.We also investigated whether KEAP1’s knockdown can stabilize nuclear factor(erythroid-derived 2)-like 2(NRF2)protein levels that led to sorafenib’s resistance,including an NRF2 inhibitor that can synergize with sorafenib to abolish HCC’s growth in vitro and in vivo.Furthermore,we clarified that fibroblast growth factor 21(FGF21)is an important downstream regulator of NRF2 in HCC.Intriguingly,we observed that FGF21 bound to NRF2 through the C-terminus of FGF21,thereby stabilizing NRF2 by reducing its ubiquitination and generating a positive feedback loop in sorafenib-resistant HCC.These findings,therefore,propose that targeting FGF21 is a promising strategy to combat HCC sorafenib’s resistance.

Change of Inflammatory Factors in Patients with Acute Coronary Syndrome

Background： Acute coronary syndrome （ACS） is closely related to unstable plaques and secondary thrombosis. The inflammatory cells in plaques and their inflammatory products may be the cause for plaque instability and ruptures. The study aimed to disclose the changes of inflammatory factors including serum intracellular adhesion molecule-1（ICAM-1 ）, chitinase-3-like protein I （YKL-40）, and lipoprotein-associated phospholipase A2 （Lp-PLA2） in patients with ACS and its clinical significance. Methods： A total of 120 patients with coronary heart disease （CHD） were categorized into 2 groups： 69 with ACS and 51 with stable angina pectoris （SAP）： 20 patients with chest pain and normal angiography served as a control group. The 120 patients with CHD were categorized into single-vessel disease group, double-vessel disease group, and three-vessel disease group based on the number of coronary artery stenosis. The severity of coronary artery stenosis was quantified based on coronary angiography using Gensini score. They were further divided into mild CHD group with its Gensini score 〈26 （n = 36）, moderate CHD group with its Gensini score being 26-54 （n = 48） and severe CHD group with its Gensini score 〉54 （n = 36）. Serum levels of ICAM-1, YKL-40, and Lp-PLA2 of different groups were determined by enzyme-linked immunosorbent assay. Correlation between ICAM-1, YKL-40, Lp-PLA2, and Gensini score was analyzed. Results： The levels of serum inflammatory factors ICAM-1, YKL-40, and Lp-PLA2 were significantly higher in the ACS group than those in control group and SAP group （all P 〈 0.05）： and compared with control group, no significant difference was observed in terms of the serum ICAM-1, YKL-40, and Lp-PLA2 levels in the SAP group （P 〉 0.05）.The levels of serum ICAM-1, YKL-40, and Lp-PLA2 were not significantly different among control group, single-vessel disease group, double-vessel disease group, and three-vessel disease group （all P 〉 0.05）. The levels of serum ICAM-1, YKL-40, and Lp-PLA2 were not significantly different among control group, mild CHD group （Gensini score 〈26）, moderate CHD group （Gensini score 26-54）, and severe CHD group （Gensini score 〉54） （all P 〉 0.05）. Nonparametric Spearman correlation analysis showed that the levels of serum ICAM-1, YKL-40, and Lp-PLA2 were not correlated with the Gensini score in CHD patients （r=0.093, r=-0.149, and r= -0.085, all P 〉 0.05; respectively）. Conclusions： The serum levels of ICAM-1, YKL-40, and Lp-PLA2 were correlated with different clinical types of CHD, but not well correlated the severity and extent of artery stenosis, suggesting that ICAM-1, YKL-40, and Lp-PLA2 rnight be involved in occurrence of instability of atherosclerotic plaque, and might reflect the severity of CHD mostly through reflecting the plaque stability.

Efficacy of Qifu Lizhong enema prescription(芪附理中灌肠方)on intestinal mucosal tight junction function modulation of ulcerative colitis rat model

OBJECTIVE:To investigate the efficacy and mechanism of Qifu Lizhong enema prescription(芪附理中灌肠方,QFLZ)on intervening ulcerative colitis(UC)rat model with TCM spleen and kidney Yang insufficiency syndrome METHODS:Seventy-two male Sprague-Dawley rats were randomly assigned to six groups:normal model,mesalazine,and QFLZ high,medium,and low dose groups,each with 12 rats.After 3 d of adaptation feeding,all groups except the normal group were induced using rhubarb decoction in combination with trinitrobenzene sulfonic acid(TNBS)/55%ethanol to establish a UC rat model.Following successful modeling,the normal and model groups received daily saline enema,while the Chinese medicine and Western medicine groups received daily QFLZ and Mesalazine enema for 2 weeks respectively.The disease activity index score,hematoxylin and eosin staining,immunohistochemistry,and Western blotting were used to determine the expression of claudin 1,claudin 2,zonula occludens-1protein(ZO-1),and F-actin proteins in each rat colon tissue following treatment.RESULTS:QFLZ significantly alleviated the structural disorganization in the form of epithelial glands in the intestinal mucosa of rats with UC and retarded the progression of the disease.The intestinal mucosal epithelial cells of UC rats showed decreased expression of claudin 1,ZO-1,F-actin(P<0.05),claudin 2 appeared elevated(P<0.05),which resulted in impaired TJ.Treatment with QFLZ resulted in elevated expression of claudin 1(P<0.05),ZO-1(P<0.05)and F-actin(P<0.05)and decreased expression of claudin 2(P<0.05),which allowed for repair of the intestinal mucosal TJ,which in turn served as a treatment for UC.CONCLUSIONS:The mechanism of repairing TJ function and repairing the intestinal mucosal barrier by QFLZ may be associated with up-regulation of claudin 1,ZO-1,and F-actin levels,and down-regulation of claudin 2 expression level.

Targeting neuronal mitophagy in ischemic stroke:an update

Cerebral ischemia is a neurological disorder associated with complex pathological mechanisms,including autophagic degradation of neuronal mitochondria,or termed mitophagy,following ischemic events.Despite being well-documented,the cellular and molecular mechanisms under-lying the regulation of neuronal mitophagy remain unknown.So far,the evidence suggests neuronal autophagy and mitophagy are separately regulated in ischemic neurons,the latter being more likely activated by reperfusional injury.Specifically,given the polarized morphology of neurons,mitophagy is regulated by different neuronal compartments,with axonal mitochondria being degraded by autophagy in the cell body following ischemia-reperfusion insult.A variety of molecules have been associated with neuronal adaptation to ischemia,including PTEN-induced kinase 1,Parkin,BCL2 and adenovirus E1B 19-kDa-interacting protein 3(Bnip3),Bnip3-like(Bnip3l)and FUN14 domain-containing 1.Moreover,it is still controversial whether mitophagy protects against or instead aggravates ischemic brain injury.Here,we review recent studies on this topic and provide an updated overview of the role and regulation of mitophagy during ischemic events.

Relationship between Two Blood Stasis Syndromes and Inflammatory Factors in Patients with Acute Coronary Syndrome

Objective： To investigate the relationship between inflammatory factors and two Chinese medicine（CM） syndrome types of qi stagnation and blood stasis（QSBS） and qi deficiency and blood stasis（QDBS） in patients with acute coronary syndrome（ACS）. Methods： Sixty subjects with ACS, whose pathogenesis changes belongs to qi disturbance blood stasis syndrome, were divided into 2 groups： 30 in the QSBS group and 30 in the QDBS group. The comparative analysis on them was carried out through comparing general information, coronary angiography and inflammatory factors including intracellular adhesion molecule-1（ICAM-1）, chitinase-3-like protein 1（YKL-40） and lipoprotein-associated phospholipase A2（Lp-PLA2）. Results： Compared with the QSBS group, Lp-PLA2 and YKL-40 levels in the QDBS group showed no-significant difference（P〉0.05）; ICAM-1 was significantly higher in the QDBS group than in the QSBS group in the pathological processes of qi disturbance and blood stasis syndrome of ACS（P〈0.05）. Conclusion： Inflammatory factor ICAM-1 may be an objective basis for syndrome typing of QSBS and QDBS, which provides a research direction for standardization research of CM syndrome types.