New advances of adiponectin in regulating obesity and related metabolic syndromes

Obesity and related metabolic syndromes have been recognized as important disease risks,in which the role of adipokines cannot be ignored.Adiponectin(ADP)is one of the key adipokines with various beneficial effects,including improving glucose and lipid metabolism,enhancing insulin sensitivity,reducing oxidative stress and inflammation,promoting ceramides degradation,and stimulating adipose tissue vascularity.Based on those,it can serve as a positive regulator in many metabolic syndromes,such as type 2 diabetes(T2D),cardiovascular diseases,non-alcoholic fatty liver disease(NAFLD),sarcopenia,neurodegenerative diseases,and certain cancers.Therefore,a promising therapeutic approach for treating various metabolic diseases may involve elevating ADP levels or activating ADP receptors.The modulation of ADP genes,multimerization,and secretion covers the main processes of ADP generation,providing a comprehensive orientation for the development of more appropriate therapeutic strategies.In order to have a deeper understanding of ADP,this paper will provide an all-encompassing review of ADP.

Study on the Correlation between Adiponectin and Bone Mineral Density in Postmenopausal Women from Guangxi Zhuang Autonomous Region

Objectives: To explore the relationship between adiponectin (APN) and bone mineral density in this Zhuang ethnic group, thus providing a basis underpinning the prevention and treatment of osteoporosis (OP). Methods: Zhuang women over 50 years old in Guangxi Zhuang Autonomous Region were included in the study. The broadband ultrasound attenuation (BUA) was adopted as the reference to calculate the T value. Quantitative ultrasonic bone density was measured on the right. Body composition measuring instrument was used to measure weight, fat, and muscle mass. Plasma APN level was detected by ELISA and blood lipids were detected by enzymatic method. Results: Plasma APN level was found with significant differences in the normal bone mineral density group, bone mineral density reduction group, and osteoporosis group (P β = −0.176, P = 0.001) when the partial correlation coefficient of APN is −0.210. Elevated APN was an independent risk factor for bone mineral density reduction (OR = 1.191, 95%CI: 1.004 - 1.407, P = 0.04) and OP (OR = 1.1337, 95%CI: 1.137 - 1.572, P Conclusion: Increased APN in postmenopausal women of Zhuang is an independent risk factor for OP. The application of APN in the OP screening and prevention of middle-aged and ageing Zhuang women still needs further research.

Growth hormone improves insulin resistance in visceral adipose tissue after duodenal-jejunal bypass by regulating adiponectin secretion

BACKGROUND The mechanism of improvement of type 2 diabetes after duodenal-jejunal bypass(DJB)surgery is not clear.AIM To study the morphological and functional changes in adipose tissue after DJB and explore the potential mechanisms contributing to postoperative insulin sensitivity improvement of adipose tissue in a diabetic male rat model.METHODS DJB and sham surgery was performed in a-high-fat-diet/streptozotocin-induced diabetic rat model.All adipose tissue was weighed and observed under microscope.Use inguinal fat to represent subcutaneous adipose tissue(SAT)and mesangial fat to represent visceral adipose tissue.RNA-sequencing was utilized to evaluate gene expression alterations adipocytes.The hematoxylin and eosin staining,reverse transcription-quantitative polymerase chain reaction,western blot,and enzyme-linked immunosorbent assay were used to study the changes.Insulin resistance was evaluated by immunofluorescence.RESULTS After DJB,whole body blood glucose metabolism and insulin sensitivity in adipose tissue improved.Fat cell volume in both visceral adipose tissue(VAT)and SAT increased.Compared to SAT,VAT showed more significantly functional alterations after DJB and KEGG analysis indicated growth hormone(GH)pathway and downstream adiponectin secretion were involved in metabolic regulation.The circulating GH and adiponectin levels and GH receptor and adiponectin levels in VAT increased.Cytological experiment showed that GH stimulated adiponectin secretion and improve insulin sensitivity.CONCLUSION GH improves insulin resistance in VAT in male diabetic rats after receiving DJB,possibly by increasing adiponectin secretion.

Adiponectin orchestrates testosterone suppression in biological pathways

This current review highlights adiponectin engagement with AdipoR1 and AdipoR2 which subsequently triggers pathways such as AMPK,PPARα,and MAPK,thereby modulating testicular steroidogenesis.Adiponectin's actions on Leydig and adrenal cells inhibit androgen secretion by suppressing the steroidogenic acute regulatory protein(StAR).Given that StAR facilitates cholesterol to testosterone conversion,AMPK inhibits this process by modulating cholesterol transport and suppressing StAR expression through multiple avenues.Furthermore,adiponectin-induced PPARαactivation impedes mitochondrial cholesterol influx,further modulating androgen biosynthesis.The suppressive influence of PPARαon steroidogenic genes,notably StAR,is evident.Collectively,adiponectin signalling predominantly attenuates androgen production,ensuring metabolic and reproductive equilibrium.Imbalances,as seen in conditions like hypogonadism and obesity-related infertility,highlight their crucial roles and potential clinical interventions for reproductive disorders.

Exercise preconditioning alleviates ischemia-induced memory deficits by increasing circulating adiponectin

Cerebral ischemia is a major health risk that requires preventive approaches in addition to drug therapy.Physical exercise enhances neurogenesis and synaptogenesis,and has been widely used for functional rehabilitation after stroke.In this study,we determined whether exercise training before disease onset can alleviate the severity of cerebral ischemia.We also examined the role of exercise-induced circulating factors in these effects.Adult mice were subjected to 14 days of treadmill exercise training before surgery for middle cerebral artery occlusion.We found that this exercise pre-conditioning strategy effectively attenuated brain infarct area,inhibited gliogenesis,protected synaptic proteins,and improved novel object and spatial memory function.Further analysis showed that circulating adiponectin plays a critical role in these preventive effects of exercise.Agonist activation of adiponectin receptors by Adipo Ron mimicked the effects of exercise,while inhibiting receptor activation abolished the exercise effects.In summary,our results suggest a crucial role of circulating adiponectin in the effects of exercise pre-conditioning in protecting against cerebral ischemia and supporting the health benefits of exercise.

Boiogito Increases the Synthesis and Secretion of Adiponectin by Promoting Differentiation in Cultured Human Adipocytes

Boiogito (BOT) ameliorates insulin resistance and diabetes in several animal models;however, the underlying mechanisms for these in vivo effects remain unclear. Thiazolidine derivatives, which are peroxisome proliferator-activated receptor γ (PPARγ) agonists for the treatment of type II diabetes, promote adiponectin production by inducing adipocyte differentiation, thereby reducing insulin resistance. This study aimed to evaluate the effect of BOT on adipocyte differentiation using cultured human visceral preadipocytes (HVPAds) compared with the thiazolidine derivative troglitazone (TRG). We investigated the effects of BOT (0.125 - 1 mg/mL) and TRG (10 μM) on the differentiation of adipocytes treated with or without tumor necrosis factor-α (TNF-α: 5 ng/mL). On day 14 of culture, the following adipocyte differentiation marker levels were measured: intracellular lipids, extracellular (i.e., medium) adiponectin, and intracellular differentiation-related genes (PPARγ, CCAAT/enhancer binding protein, adiponectin, differentiation cluster 36, glucose transporter type 4). BOT and TRG increased factors associated with differentiation including lipid, adiponectin, and differentiation-related gene expression levels compared with the controls. The increases in these differentiation markers were inhibited by the PPARγ antagonist GW9662 (20 μM). Furthermore, TNF-α decreased all differentiation marker levels. The decreases in differentiation markers were inhibited by BOT and TRG;however, these inhibitory effects were blocked by GW9662. The results suggest that BOT increases the synthesis and secretion of adiponectin by promoting differentiation similar to TRG. This study is the first to demonstrate that adipocyte differentiation-promoting activity is a mechanism for the beneficial effects of BOT on diabetes and insulin resistance.

Adiponectin as a therapeutic target for diabetic foot ulcer

The global burden of diabetic foot ulcers(DFUs)is a significant public health concern,affecting millions of people worldwide.These wounds cause considerable suffering and have a high economic cost.Therefore,there is a need for effective strategies to prevent and treat DFUs.One promising therapeutic approach is the use of adiponectin,a hormone primarily produced and secreted by adipose tissue.Adiponectin has demonstrated anti-inflammatory and antiatherogenic properties,and researchers have suggested its potential therapeutic applications in the treatment of DFUs.Studies have indicated that adiponectin can inhibit the production of pro-inflammatory cytokines,increase the production of vascular endothelial growth factor,a key mediator of angiogenesis,and inhibit the activation of the intrinsic apoptotic pathway.Additionally,adiponectin has been found to possess antioxidant properties and impact glucose metabolism,the immune system,extracellular matrix remodeling,and nerve function.The objective of this review is to summarize the current state of research on the potential role of adiponectin in the treatment of DFUs and to identify areas where further research is needed in order to fully understand the effects of adiponectin on DFUs and to establish its safety and efficacy as a treatment for DFUs in the clinical setting.This will provide a deeper understanding of the underlying mechanisms of DFUs that can aid in the development of new and more effective treatment strategies.

2型糖尿病视网膜病变患者中医证型分布及其与血清炎症因子及脂联素水平的相关性研究

【目的】探讨2型糖尿病视网膜病变(type 2 diabetic retinopathy,T2DR)的中医证型分布及其与血清炎症因子、脂联素(APN)水平的相关性,为T2DR的中医辨证分型提供客观依据。【方法】采用横断面病例对照研究方法,选择2022年9月至2023年3月在江西省赣州市人民医院眼科诊断为T2DR的患者共42例84眼,观察T2DR患者眼底荧光血管造影(FFA)分期与中医辨证分型的关系,分析不同中医证型与血清炎症因子及APN水平的关系以及不同FFA分期的血清炎症因子及APN水平差异,探讨T2DR患者各变量与不同中医证型之间的相关性。【结果】(1)42例T2DR患者中,男性27例,女性15例,平均年龄为(54.0±12.0)岁;其中,肝肾亏虚、目络失养证14例(33.3%),阴精不足、燥热内生证15例(35.7%),气阴两虚、络脉瘀阻证9例(21.4%),阴阳两虚、血瘀痰凝证4例(9.5%),脾失健运、水湿阻滞证0例(0.0%)。(2)肝肾亏虚、目络失养证患者中双眼眼底FFA分期≥4期[增殖期糖尿病视网膜病变(PDR)]者占78.6%(11/14),阴精不足、燥热内生证患者占73.3%(11/15),气阴两虚、络脉瘀阻证患者和阴阳两虚、血瘀痰凝证患者均占100%(9/9;4/4),但组间比较,差异无统计学意义(P=0.272)。(3)42例T2DR患者中,有35例(83.3%)患者的肿瘤坏死因子α(TNF-α)、28例(68.3%)患者的C反应蛋白(CRP)、38例(90.5%)患者的糖化血红蛋白(HbA1c)水平均高于正常值;但不同FFA分期患者的血清炎症因子TNF-α、CRP、白细胞介素6(IL-6)、血管内皮生长因子(VEGF)及APN、HbA1c水平比较,差异均无统计学意义(P>0.05);同时,不同中医证型的血清APN、TNF-α、CRP、IL-6、VEGF水平比较,差异也均无统计学意义(P>0.05)。(4)相比肝肾亏虚、目络失养证患者,阴阳两虚、血瘀痰凝证患者的眼部病程较短,两者的相关性接近差异有统计学意义(r=-0.467,P=0.051);相比阴精不足、燥热内生证患者,阴阳两虚、血瘀痰凝证患者的CRP水平较高(r=0.592,P=0.010);相比气阴两虚、络脉瘀阻证患者,阴阳两虚、血瘀痰凝证患者的CRP水平较高(r=0.668,P=0.013)和糖尿病病程更长(r=0.629,P=0.021)。【结论】血清TNF-α及CRP在T2DR中有更高的表达;肝肾亏虚、目络失养证和阴精不足、燥热内生证为T2DR的常见证型;阴阳两虚、血瘀痰凝证与CRP密切相关,同时阴阳两虚、血瘀痰凝证型患者有更长的糖尿病病程。

血清脂联素、成纤维生长因子-23在心脏瓣膜置换术患者预后中的评估价值

目的探讨血清脂联素、成纤维生长因子-23(FGF23)水平在心脏瓣膜置换术患者预后中的评估价值。方法选取行心脏瓣膜置换术的患者98例为研究组。根据研究组患者的预后情况分为预后良好组(n=67)和预后不良组(n=31)。选取同期健康体检者90例为对照组。采用Spearman法分析血清脂联素、FGF23水平分别与血浆N末端B型利钠肽前体(NT-proBNP)水平和急性生理学与慢性健康状况评分系统Ⅱ(APACHEⅡ)评分的相关性。采用多因素Logistic回归分析法分析心脏瓣膜置换术患者预后的影响因素。绘制受试者工作特征(ROC)曲线分析血清脂联素、FGF23水平对心脏瓣膜置换术患者预后的预测价值。结果研究组血清FGF23、NT-proBNP水平、APACHEⅡ评分高于对照组,血清脂联素水平低于对照组,差异有统计学意义(P<0.05)。预后不良组血清FGF23、NT-proBNP水平和APACHEⅡ评分高于预后良好组,血清脂联素水平低于预后良好组,差异有统计学意义(P<0.05)。患者的血清FGF23水平与NT-proBNP水平、APACHEⅡ评分呈正相关(P<0.05)。血清脂联素水平与NT-proBNP水平、APACHEⅡ评分呈负相关(P<0.05)。血清脂联素、FGF23、NT-proBNP水平和APACHEⅡ评分为心脏瓣膜置换术患者预后的影响因素(P<0.05)。血清脂联素、FGF23单独预测和联合预测心脏瓣膜置换术患者预后的曲线下面积(AUC)分别为0.862、0.807、0.911。脂联素、FGF23联合预测的AUC大于单独预测,差异有统计学意义(P<0.05)。结论血清脂联素、FGF23联合预测心脏瓣膜置换术患者预后的效果较好。血清脂联素、FGF23有望成为评估心脏瓣膜置换术患者预后效果的有效指标。

脂联素干预对宫腔粘连大鼠子宫内膜组织中NLRP3、TGF-β1和Smad2表达的影响

目的:探讨脂联素干预对宫腔粘连大鼠子宫内膜组织中NLRP3、TGF-β1和Smad2表达的影响。方法:健康雌性SD大鼠24只采用双重损伤法建立宫腔粘连模型后,随机平均分为模型组(腹腔注射生理盐水1 mL/d)和脂联素组[腹腔注射脂联素蛋白10μg/(kg·d)+生理盐水1 mL/d],连续干预14 d;12只未造模大鼠为正常对照组。末次给药后,麻醉大鼠,收取子宫组织,HE染色及Masson染色法检测子宫内膜腺体数量和纤维化面积百分比,免疫组化、Western blot及RT-qPCR法检测NLRP3、TGF-β1及Smad2蛋白和mRNA的表达。结果:正常对照组、模型组和脂联素组子宫内膜腺体数分别为(55.1±5.6)、(13.8±4.5)和(33.7±7.8),纤维化面积百分比分别为(5.39±0.65)%、(65.18±1.92)%和(38.16±1.91)%;与正常对照组比较,模型组腺体数减少,纤维化面积百分比增加(P<0.05);与模型组比较,脂联素组腺体数增加,纤维化面积百分比减少(P<0.05)。模型组和脂联素组子宫内膜组织中NLRP3、TGF-β1和Smad2蛋白和mRNA的表达均高于正常对照组(P<0.05);脂联素组低于模型组(P<0.05)。结论:脂联素可能通过抑制NLRP3炎症小体的激活和TGF-β1/Smad2信号通路,减轻宫腔粘连大鼠子宫内膜炎症,从而抑制纤维化进展。

腹腔镜胃袖状切除术治疗肥胖症的效果及对血清瘦素、脂联素水平的影响

目的分析腹腔镜胃袖状切除术(LSG)治疗肥胖症的效果及对血清瘦素、脂联素水平的影响。方法纳入50例行LSG治疗的肥胖症患者,统计患者的手术情况(手术时间、术中出血量、术后肛门排气时间、术后住院时间)。术后随访6个月,比较患者术前和术后1个月、3个月、6个月的血清瘦素、脂联素水平及减重指标[体重、体质指数、多余体重减少百分比(EWL%)、腰围]。统计患者术后6个月内不良反应的发生情况及合并症的改善情况。结果50例患者均顺利完成手术,手术时间为70~160(118.6±20.4)min,术中出血量为24~75(48.3±18.7)mL,术后肛门排气时间为2~4(2.3±0.5)d,术后住院天数为4~10(8.2±2.4)d。患者的血清瘦素、脂联素水平及体重、体质指数、EWL%、腰围均有随时间变化的趋势(P<0.05),其中,术后1个月、3个月、6个月,患者血清瘦素水平、体重、体质指数、腰围低于术前,血清脂联素水平高于术前,术后EWL%呈逐渐升高的趋势(P<0.05)。术后6个月,仅有1例患者出现肺部感染,患者的合并疾病均得到明显改善。结论LSG治疗肥胖症的效果显著,可明显改善患者的血清瘦素和脂联素水平,还可以改善肥胖症的合并疾病,临床效果较好。

脂联素、瘦素、Pref-1与胰岛素抵抗关系及联合检测预测糖尿病前期病情进展风险的效能

目的探讨脂联素、瘦素、前脂肪细胞因子-1(Pref-1)与胰岛素抵抗的关系及联合检测预测糖尿病前期病情进展风险的效能。方法选取2019年1月至2023年1月郑州大学第一附属医院收治的304例糖尿病前期患者进行前瞻性队列研究。根据1年内是否进展为糖尿病分为糖尿病组(62例)、糖尿病前期组(242例),另选同期正常糖耐量人群60例作为对照组。比较三组受检者的基线资料及血清脂联素、瘦素、Pref-1表达水平,采用Pearson法分析血清脂联素、瘦素、Pref-1水平与胰岛素抵抗(IR)的相关性,采用Logistic回归分析血清脂联素、瘦素、Pref-1水平对糖尿病前期病情进展的影响,采用受试者工作特征曲线(ROC)分析血清脂联素、瘦素、Pref-1单独及联合检测对糖尿病前期病情进展风险的预测效能。结果三组受检者的年龄、体质量指数(BMI)、甘油三酯、空腹血糖、胰岛素抵抗指数(HOMA-IR)比较,糖尿病组高于糖尿病前期组,且糖尿病前期组高于对照组,差异均有统计学意义(P<0.05);糖尿病组患者的脂联素、Pref-1分别为(2.82±0.93)mg/L、(0.30±0.10)μg/L,明显低于糖尿病前期组的(6.76±2.17)mg/L、(0.51±0.16)μg/L,且糖尿病前期组患者的脂联素、Pref-1明显低于对照组的(8.45±2.80)mg/L、(0.84±0.27)μg/L,而糖尿病组患者的瘦素为(12.00±2.98)μg/L,明显高于糖尿病前期组的(8.79±2.87)μg/L,且糖尿病前期组患者的瘦素明显高于对照组的(3.56±1.09)μg/L,差异均有统计学意义(P<0.05);脂联素(r=-0.694)、Pref-1(r=-0.853)与HOMA-IR呈负相关(P<0.05),瘦素(r=0.660)与HOMA-IR呈正相关(P<0.05);Logistic回归分析结果显示,年龄、BMI、甘油三酯、空腹血糖、脂联素、瘦素、Pref-1是糖尿病前期患者病情进展的独立影响因素,将年龄、BMI、甘油三酯、空腹血糖进行校正,以脂联素、瘦素、Pref-1作为自变量,脂联素、瘦素、Pref-1仍是糖尿病前期患者病情进展的独立影响因素(P<0.05);ROC曲线分析结果显示,脂联素预测糖尿病前期病情进展风险的曲线下面积(AUC)为0.730,截断值≤3.51 mg/L,敏感度为79.03%,特异度为59.09%,瘦素预测的AUC为0.760,截断值>10.78μg/L,敏感度为67.74%,特异度为73.55%,Pref-1预测的AUC为0.795,截断值≤0.37μg/L,敏感度为80.65%,特异度为65.70%,且联合检测预测糖尿病前期病情进展的AUC为0.904,敏感度为87.10%,特异度为82.23%(P<0.05)。结论血清脂肪因子脂联素、Pref-1与不同糖耐量受损人群IR呈负相关,瘦素与之呈正相关,且联合检测对糖尿病前期病情进展风险具有一定预测价值,可作为临床早期预测病情进展风险的辅助指标。

脂联素基因多态性与直肠腺瘤切除预后相关性分析

目的:探讨脂联素(APN)基因多态性与直肠腺瘤(RA)切除预后的相关性。方法:选取接受切除手术治疗的RA病人97例,根据预后情况,将复发RA病人52例作为观察组,无复发病人45例作为对照组。通过聚合酶链式反应-限制性片段长度多态性(PCR-RELP)法检测受试者血清中APN基因rs2241766位点多态性基因分布频率,并分析APN单核苷酸多态性各基因型与RA切除预后的相关性。结果:APN基因rs2241766位点基因型有TT野生型、TG杂合子型、GG纯合子型,对照组与观察组APN基因rs2241766位点基因型符合Hardy-Weinberg平衡定律,2组APN基因rs2241766位点基因型及等位基因频率差异均有统计学意义(P<0.01)。突变杂合子TG型、突变纯合子GG型病人的腺瘤数、腺瘤最大径及平均直径均大于野生TT型(P<0.05),纯合子GG型病人腺瘤数、腺瘤最大径及平均直径均大于杂合子TG型(P<0.05)。二元logistic回归分析显示,APN基因rs2241766位点TG型、GG型突变均为RA切除后复发的危险因素(P<0.01)。结论:APN基因rs2241766位点多态性与RA切除预后具有相关性。

急性痛风性关节炎患者外周血脂联素与CD4^(+)T细胞亚群的分析及相关性研究

目的比较急性痛风性关节炎患者与健康对照组外周血脂联素及CD4+T细胞亚群的差异,并探究痛风患者脂联素与血尿酸、疾病活动度、CT4^(+)T细胞亚群及部分细胞因子的相关性。方法收集急性痛风组(n=90)及健康对照组(n=72)的临床资料(包括一般资料、中性粒细胞、红细胞沉降率、C反应蛋白、血尿酸、CT4^(+)T细胞亚群及部分细胞因子);检测两组外周血脂联素水平,比较两组间外周血脂联素及CD4+T细胞亚群的差异;分析脂联素与各临床资料的相关性。结果与健康对照组比较,急性痛风组外周血脂联素水平明显降低(P<0.001),且Th2、Th17、Th17/Treg均升高(P<0.05),Treg、Th1/Th2均降低(P<0.05)。急性痛风组外周血脂联素与中性粒细胞、红细胞沉降率及C反应蛋白均呈负相关(r=-0.244,P<0.05;r=-0.311,P<0.05;r=-0.506,P<0.001),而与血尿酸无相关性。急性痛风组外周血脂联素与Th1和Th1/Th2均呈正相关(r=0.252,P<0.05;r=0.218,P<0.05)。急性痛风组外周血脂联素与白细胞介素-2(interleukin-2,IL-2)、白细胞介素-4(interleukin-4,IL-4)和白细胞介素-10(interleukin-10,IL-10)均呈正相关(r=0.323,P<0.05;r=0.377,P<0.05;r=0.359,P<0.05);而与白细胞介素-6(interleukin-6,IL-6)和肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)呈负相关(r=-0.265,P<0.05;r=-0.299,P<0.05)。多元线性回归分析显示,急性痛风组外周血脂联素与红细胞沉降率、C反应蛋白、IL-6及TNF-α均呈负相关(B _(ESR)=-12.541,P=0.003;B_( CRP)=-8.256,P=0.024;B_( IL-6)=-15.907,P=0.037;B _(TNF-α)=-79.770,P=0.040),而与Th1呈正相关(B _(Th1)=2.959,P=0.006)。结论急性痛风性关节炎患者外周血脂联素水平降低,Th2和Th17升高,而Treg降低,脂联素降低与急性痛风性关节炎患者免疫紊乱及免疫炎症相关。

慢性牙周炎患者入院时血清脂联素、瘦素水平与疾病严重程度的关系

目的探讨慢性牙周炎(CP)患者血清脂联素(ADPN)、瘦素(LEP)的表达及与疾病严重程度的关系。方法前瞻性纳入郑州大学第一附属医院2021年3月至2023年3月收治的90例CP患者为研究组,并依据入院时疾病严重程度分为轻度组(48例)、中度组(28例)、重度组(14例),另选取同期至医院体检的90例健康人群作为对照组。对比研究组与对照组、不同疾病严重程度CP患者间的血清ADPN、LEP水平及其他临床资料。结果研究组血清LEP水平高于对照组,ADPN水平低于对照组(P<0.05)。重度组、中度组、轻度组患者LEP、既往吸烟史占比依次降低,ADPN水平依次升高(P<0.05)。经点二列相关性分析显示,血清LEP与CP患者疾病严重程度呈正相关(r>0,P<0.05);血清ADPN、既往吸烟史与CP患者疾病严重程度呈负相关(r<0,P<0.05)。结论血清ADPN、LEP在CP患者中呈异常表达,且随着病情严重程度的提升,ADPN水平下降,LEP水平升高。

止血散瘀明目汤联合全视网膜激光光凝对糖尿病视网膜病变患者视力、黄斑厚度及血清脂联素水平的影响

【目的】探讨止血散瘀明目汤(由黄芪、牡丹皮、山药、知母、黄柏、生地黄等中药组成)联合全视网膜激光光凝(PRP)对糖尿病视网膜病变(DR)患者视力、黄斑厚度及血清脂联素水平的影响。【方法】回顾性分析2020年2月至2022年5月收治的98例气阴两虚、脉络瘀滞型DR患者的临床资料,根据治疗方式的不同分成PRP组48例和联合组50例。PRP组单纯给予PRP治疗,联合组在PRP治疗基础上联合止血散瘀明目汤治疗,疗程为3个月。观察2组患者治疗前和治疗3个月后中医证候积分、视力、黄斑厚度、视网膜中央静脉(CRV)血流相关参数[舒张末期血流速度(EDV)、收缩期峰值血流速度(PSV)]、血脂指标及血清脂联素水平的变化情况。【结果】(1)治疗3个月后,2组患者的中医证候积分、黄斑厚度均较治疗前明显降低(P<0.05),视力均较治疗前明显升高(P<0.05),且联合组治疗后的中医证候积分、黄斑厚度明显低于PRP组,视力明显高于PRP组,差异均有统计学意义(P<0.01)。(2)治疗3个月后,2组患者的CRV血流相关参数EDV、PSV均较治疗前明显升高(P<0.05),且联合组的EDV、PSV均明显高于PRP组,差异均有统计学意义(P<0.01)。(3)治疗3个月后,联合组的总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)水平均较治疗前降低(P<0.05),而PRP组的TC、LDL-C水平均无显著性改变(P>0.05);治疗后组间比较,联合组的TC、LDL-C水平均明显低于PRP组,差异均有统计学意义(P<0.01)。(4)治疗3个月后,2组患者的血清脂联素水平均较治疗前升高(P<0.01),且联合组治疗后的血清脂联素水平明显高于PRP组,差异有统计学意义(P<0.01)。【结论】针对气阴两虚、脉络瘀滞型DR患者,在PRP治疗基础上联合止血散瘀明目汤治疗,可有效上调血清脂联素水平,明显减小黄斑厚度,显著改善血脂指标、CRV血流相关参数及患者视力。

急性脑梗死患者血清中高迁移率族蛋白、脂联素和氧化低密度脂蛋白的表达水平及其与颈动脉粥样硬化的相关性

目的探讨急性脑梗死患者颈动脉粥样硬化与血清中高迁移率族蛋白(HMGB)、脂联素和氧化低密度脂蛋白(oxLDL)表达水平的相关性。方法回顾性选取2021年9月至2023年9月唐山市人民医院收治的80例急性脑梗死患者作为急性脑梗死组,梗死类型:轻度梗死(梗死直径<3.0 cm)30例,中度梗死(梗死直径3.0~5.0 cm)30例,重度梗死(梗死直径>5.0 cm)20例;颈动脉粥样硬化:内膜粗糙28例,稳定斑块36例,不稳定斑块16例;选取80名无脑血管梗死的体检老年人作为对照组。检测两组研究对象血清中HMGB、脂联素和oxLDL的表达水平,并比较不同梗死类型、不同颈动脉粥样硬化急性脑梗死患者的血清中HMGB、脂联素和oxLDL表达水平,分析急性脑梗死患者颈动脉粥样硬化与血清中HMGB、脂联素和oxLDL表达水平的相关性。结果急性脑梗死组患者的血清中HMGB和oxLDL的表达水平分别为(25.47±5.15)ng/L、(5.22±1.04)mU/L,均明显高于对照组[(3.61±1.21)ng/L、(2.61±0.45)mU/L],脂联素的表达水平为(9.52±1.25)mg/L,明显低于对照组[(17.17±2.16)mg/L],差异均有统计学意义(P<0.05)。轻度梗死、中度梗死、重度梗死急性脑梗死患者的血清中HMGB和oxLDL的表达水平均逐渐升高,脂联素的表达水平逐渐降低,差异均有统计学意义(P<0.05)。内膜粗糙、稳定斑块、不稳定斑块急性脑梗死患者的血清中HMGB和oxLDL的表达水平均逐渐升高,脂联素的表达水平逐渐降低,差异均有统计学意义(P<0.05)。急性脑梗死患者颈动脉粥样硬化程度与血清中HMGB和oxLDL的表达水平均呈显著正相关(r=0.503、0.532,P<0.05),与脂联素表达水平呈显著负相关(r=-0.601,P<0.05)。结论急性脑梗死患者血清中HMGB和oxLDL的表达水平明显升高,脂联素的表达水平明显降低,血清HMGB、脂联素和oxLDL的表达水平与颈动脉粥样硬化病情显著相关,将有效依据提供给了临床诊治急性脑梗死。

血清脂联素对急性冠脉综合征患者介入术后不良心血管事件的预测价值

目的探讨血清脂联素(APN)对急性冠脉综合征(ACS)患者术后不良心血管事件的预测价值。方法纳入2020年4月至2022年4月在医院接受经皮冠状动脉介入治疗(PCI)的ACS患者为研究对象,于术前及术后7、30 d检测患者血清APN水平。术后随访12个月,统计术后不良心血管事件发生情况并将患者分为发生组、未发生组,比较两组术前及术后7、30 d的血清APN水平,绘制受试者工作特征(ROC)曲线,分析血清APN对ACS患者PCI后不良心血管事件的预测价值。结果完成随访工作共238例。238例ACS患者PCI后发生不良心血管事件共31例,占比13.03%。发生组2型糖尿病(T2DM)、合并冠状动脉微血管功能障碍(CMD)占比高于未发生组(P<0.05)。发生组术前及术后7、30 d血清APN水平逐渐降低,且发生组上述各时点血清APN水平均低于未发生组(P<0.05)。经多因素logistic回归分析,结果显示,血清APN低是ACS患者PCI后发生不良心血管事件影响因素(OR<1,P<0.05)。ROC曲线结果显示,术前及术后7、30 d血清APN预测ACS患者PCI后不良心血管事件的曲线下面积(AUC)均≥0.7,均有一定的预测价值。结论血清APN水平低是ACS患者PCI后发生不良心血管事件的影响因素,早期检测血清APN可以预测患者术后不良心血管事件发生风险。

运动训练对创伤后应激障碍小鼠焦虑和抑郁样行为的影响

目的:探讨运动缓解创伤后应激障碍(PTSD)焦虑抑郁样行为的作用及促进海马神经再生的中枢调控机制。方法:将雄性C57BL/6J小鼠随机分为对照组(Control)、PTSD建模组(PTSD)、建模后低强度运动组(PTSD+LE)和建模后高强度运动组(PTSD+HE)。采用条件性足部电击(CF)和单次-持续应激(SPS)相结合的方法,构建PTSD复合应激模型。利用旷场实验和悬尾实验分别评估小鼠的焦虑和抑郁样行为。通过免疫荧光双标实验观察小鼠海马DG区新生成熟神经元和增殖细胞。采用Western Blot检测小鼠海马脂联素受体1(AdipoR1)的表达情况。结果:旷场实验结果表明PTSD+HE组小鼠在中央区域的活动距离以及逗留时间明显长于PTSD组及PTSD+LE组(P<0.05);悬尾实验结果显示与PTSD组小鼠相比,不同程度运动训练组小鼠的不动时间明显减少(P<0.05),而且PTSD+HE组更显著(P<0.05)。此外,PTSD+HE组小鼠海马DG区的BrdU+、BrdU+/NeuN+与MCM2+细胞密度明显升高(P<0.05)。PTSD+HE组小鼠海马AdipoR1蛋白表达明显上调(P<0.05)。结论:PTSD小鼠焦虑和抑郁样行为与海马神经再生水平下降有关。运动可改善其焦虑和抑郁样行为,作用机制可能与促进AdipoR1表达、促进海马神经再生有关。

Adiponectin基因剔除LacZ基因敲入小鼠模型的建立

adiponectin是脂肪细胞特异分泌的一种活性蛋白质,具有增加胰岛素敏感性、抗炎及抗动脉硬化等活性.建立adiponectin基因剔除β-半乳糖苷酶基因(LacZ)敲入小鼠模型,可为整体动物水平研究adiponectin基因功能及其表达调控机制等提供理想工具.根据生物信息学方法获得adiponectin基因组序列,设计基因剔除及敲入策略,在adiponectin基因第2和第3号外显子剔除的同时,在其ATG和信号肽序列后顺接LacZ基因完整编码序列,构建完成了Adipo-LacZ-XpPNT基因剔除质粒.通过电穿孔将打靶质粒转入ES细胞,以G418和ganciclovir进行药物筛选,获得药物抗性的ES细胞克隆,PCR和DNA印迹鉴定出正确同源重组克隆.将同源重组的ES细胞克隆注入小鼠囊胚得到嵌合体小鼠,嵌合体小鼠与C57BL/6J小鼠交配产生杂合子小鼠,杂合子间交配获得adiponectin基因剔除LacZ基因敲入纯合子小鼠.经RT-PCR、RNA印迹和ELISA检测证实纯合子小鼠脂肪和血清中adiponectin基因表达呈阴性.RT-PCR、RNA印迹及蛋白质印迹检测发现,LacZ基因在突变小鼠脂肪组织中有特异性表达,其表达谱与内源性adiponectin基因的表达谱一致.但在脂肪组织及外周血中未能检测到LacZ活性,且血清中LacZ蛋白亦呈阴性.由此成功建立了adiponectin基因完全灭活及LacZ基因以内源性adiponectin基因表达谱表达的小鼠模型,为进一步研究该基因功能及其表达调控创造了有利条件.