Protective Effects of a Hydrogen-Rich Preservation Solution in a Canine Lung Transplantation Model

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急性脑梗死患者血清CTRP3,CTRP9水平与颈总动脉内膜中层厚度的相关性分析

目的 探讨急性脑梗死(Acute cerebral infarction,ACI)患者血清中补体C1q/肿瘤坏死因子相关蛋白3/9(Complement-C1q/tumor necrosis factor-related protein 3/9,CTRP3/9)的水平变化及其与颈总动脉内膜中层厚度(Carotid intima-media thickness,CIMT)的相关性。方法 选取2015年12月-2019年1月本院收治的102例ACI患者进行研究(ACI组),并选取同时间段内98例体检健康者进行对照分析研究(对照组); 分析比较2组受试者一般资料; 采用酶联免疫吸附法(Enzyme linked immunosorbent assay,ELISA)检测2组受试者血清CTRP3,CTRP9水平; 利用彩色多普勒超声仪检测2组受试者CIMT; Pearson法分析ACI患者血清CTRP3,CTRP9水平与CIMT以及CTRP3与CTRP9水平的关系; 采用Logistic回归分析法ACI患者CIMT的影响因素。结果 ACI组血清低密度脂蛋白-胆固醇(Low density lipoprotein cholesterol,LDL-C)、总胆固醇(Total cholesterol,TC)、甘油三酯(Triglyceride,TG)水平均高于对照组(P<0.05),血清CTRP3,CTRP9、高密度脂蛋白-胆固醇(HDL-C)水平明显均明显低于对照组(P<0.05),CIMT较对照组增加(P<0.05); ACI患者血清CTRP3与CTRP9水平呈正相关(r=0.490,P<0.05),血清CTRP3,CTRP9水平与CIMT均呈负相关(r=-0.461、-0.482,P<0.05); TG,TC,LDL-C水平为ACI患者CIMT增加的危险因素(P<0.05),HDL-C,CTRP3,CTRP9水平为ACI患者CIMT增加的保护因素(P<0.05)。结论 ACI患者血清CTRP3,CTRP9水平均明显降低,两者可能与CIMT相互影响,共同影响ACI发生发展。     

腹腔镜经胃胰腺坏死组织清除治疗包裹性胰腺坏死32例疗效分析

目的 探讨腹腔镜经胃胰腺坏死组织清除（LTGD）治疗包裹性胰腺坏死（WOPN）的安全性及有效性。方法 回顾性分析2011年1月至2020年12月在首都医科大学宣武医院接受LTGD治疗的32例病人资料。记录手术时间、术后住院时间、围手术期及远期并发症发生情况。结果 32例WOPN病人中，28例（87.5%）局限于胰腺或胰周，23例（71.9%）合并脾静脉血栓及左侧门静脉高压。手术时距离发病45（27~181）d。手术时间（151±32） min，出血量（75±40） mL, 术后住院时间12（6～43）d，术后并发症发生率为21.9%（7/32），Clavien-Dindo Ⅲ级及以上并发症发生率为15.6%，死亡率为3.13%。中位随访时间52（6～101）个月，27例（84.4%）病人成功获得随访，所有WOPN均吸收，无复发。随访期内，胰腺内、外分泌功能障碍发生率分别为18.5%（5/27）及14.8%（4/27）。结论 对局限于胰腺或胰周的WOPN，LTGD是安全、有效的治疗方式。     

MiR-92b-3p ameliorates inflammation and autophagy by targeting TRAF3 and suppressing MKK3-p38 pathway in caerulein-induced AR42J cells

Acute pancreatitis (AP) is an inflammatory disease with high morbidity and mortality. Dysregulation of microRNAs (miRNAs) was involved in human diseases, including AP. However, the effects of miR-92b-3p on AP process and its mechanism remain not been fully clarified. The expression levels of miR-92b-3p and tumor necrosis factor receptor-associated factor-3 (TRAF3) were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of TRAF3, tumor necrosis factor α (TNF-α) TNF-α, interleukin-6 (IL-6), phosphorylated mitogen-activated protein kinase kinase 3 (p-MKK3), MKK3, p38 and phosphorylated p38 (p-p38) were detected by western blot. The concentration of TNF-α and IL-6 in the medium was measured using ELISA kits. The possible binding sites of miR-92b-3p and TRAF3 were predicted by TargetScan and verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The expression level of miR-92b-3p was decreased and TRAF3 expression was increased in AR42J cells stimulated with caerulein. Moreover, the protein levels of pro-inflammatory cytokines (TNF-α and IL-6) were markedly elevated, and the expression levels of autophagy-related markers Beclin1 as well as the ratio of LC3-II/I were obviously increased in AR42J cells treated with caerulein. In addition, overexpression of miR-92b-3p or knockdown of TRAF3 significantly suppressed the release of pro-inflammatory cytokines and autophagy in caerulein-induced AR42J cells. Furthermore, TRAF3 was a direct target of miR-92b-3p and its upregulation reversed the effects of miR-92b-3p overexpression on inflammatory response and autophagy. Besides, overexpression of miR-92b-3p inhibited the activation of the MKK3-p38 pathway by affecting TRAF3 expression. In conclusion, miR-92b-3p attenuated inflammatory response and autophagy by downregulating TRAF3 and suppressing MKK3-p38 pathway in caerulein-induced AR42J cells, providing a novel avenue for treatment of AP.     

肿瘤坏死因子α增强全反式维甲酸诱导早幼粒白血病细胞凋亡

目的:分析肿瘤坏死因子α增强全反式维甲酸诱导早幼粒白血病细胞凋亡的作用。方法:选择NB4人急性早幼粒白血病细胞，利用全反式维甲酸单独作用，并选择肿瘤坏死因子α联合全反式维甲酸作用，测定细胞增殖以及细胞凋亡情况。结果:随着早幼粒白血病细胞分化的逐渐进行，单一组、联合组的细胞增殖速度均慢慢下降；随着早幼粒白血病细胞分化的逐渐加深，单一组、联合组细胞凋亡率慢慢升高；分化2天，联合组细胞CD11b阳性率明显高于单一组，P<0.05。结论:全反式维甲酸具有诱导早幼粒白血病细胞分化、凋亡的作用，而肿瘤坏死因子α会增强全反式维甲酸的作用效果。     

Low-dose naltrexone inhibits the epithelial-mesenchymal transition of cervical cancer cells in vitro and effects indirectly on tumor-associated macrophages in vivo

The metastasis of cervical cancer has always been a clinical challenge. We investigated the effects of low-dose naltrexone (LDN) on the epithelial mesenchymal transition of cervical cancer cells in vitro as well as its influence on macrophage polarization and associated cytokines in vivo. The results suggested that LDN supressed the proliferation, migration and invasion abilities and promote their apoptosis in Hela cells, whereas the opioid growth factor receptor (OGFr) silenced significantly reversed these effects in vitro. Knockdown the expression of OGFr, the inhibitory of LDN on EMT was weakened. LDN could inhibit cervical cancer progression in nude mice. In additon, LDN indirectly reduced the number of tumor-associated macrophages (TAMs), mainly M2 macrophages, and decreased expression of anti-inflammatory factor IL-10 in the serum of nude mice. These findings demonstrate that LDN could be a potential treatment for cervical cancer.     

Notch1 contributes to TNF-α-induced proliferation and migration of airway smooth muscle cells through regulation of the Hes1/PTEN axis

Notch1 has been implicated in asthma pathogenesis. However, the function of Notch1 in regulating airway smooth muscle (ASM) cell proliferation and migration during airway remodeling of asthma remains unknown. Using an in vitro model induced by tumor necrosis factor (TNF)-α, we reported in this study that Notch1 participated in TNF-α-induced proliferation and migration of ASM cells. Our results demonstrated that Notch1 expression was significantly upregulated in ASM cells exposed to TNF-α. Notch1 inhibition significantly repressed TNF-α-induced ASM cell proliferation and migration, while Notch1 overexpression promoted the opposite effect. Moreover, Notch1 inhibition downregulated the expression of Notch-1 intracellular domain (NICD) and Hes1, while upregulated PTEN expression in TNF-α-exposed cells. Notably, Hes1 overexpression partially reversed the Notch1-inhibition-mediated inhibitory effect on TNF-α-induced ASM cell proliferation and migration. In addition, the promoting effect of Notch1 inhibition on PTEN expression was markedly abrogated by Hes1 overexpression. Overall, these findings demonstrated that Notch1 inhibition repressed TNF-α-induced ASM cell proliferation and migration by modulating the Hes1/PTEN signaling axis, a finding that highlights the involvement of Notch1/Hes1/PTEN in regulating airway remodeling of asthma.     

Nano-curcumin therapy,a promising method in modulating inflammatory cytokines in COVID-19 patients

BackgroundAs an ongoing worldwide health issue, Coronavirus disease 2019 (COVID–19) has been causing serious complications, including pneumonia, acute respiratory distress syndrome (ARDS), and multi-organ failure. However, there is no decisive treatment approach available for this disorder, which is primarily attributed to the large amount of inflammatory cytokine production. We aimed to identify the effects of Nano-curcumin on the modulation of inflammatory cytokines in COVID-19 patients.MethodForty COVID-19 patients and 40 healthy controls were recruited and evaluated for inflammatory cytokine expression and secretion. Subsequently, COVID-19 patients were divided into two groups: 20 patients receiving Nano-curcumin and 20 patients as the placebo group. The mRNA expression and cytokine secretion levels of IL-1β, IL-6, TNF-α and IL‐18 were assessed by Real‐time PCR and ELISA, respectively.ResultOur primary results indicated that the mRNA expression and cytokine secretion of IL-1β, IL-6, TNF-α, and IL-18 were increased significantly in COVID-19 patients compared with healthy control group. After treatment with Nano-curcumin, a significant decrease in IL-6 expression and secretion in serum and in supernatant (P = 0.0003, 0.0038, and 0.0001, respectively) and IL-1β gene expression and secretion level in serum and supernatant (P = 0.0017, 0.0082, and 0.0041, respectively) was observed. However, IL-18 mRNA expression and TNF-α concentration were not influenced by Nano-curcumin.ConclusionNano-curcumin, as an anti-inflammatory herbal based agent, may be able to modulate the increased rate of inflammatory cytokines especially IL-1β and IL-6 mRNA expression and cytokine secretion in COVID-19 patients, which may cause an improvement in clinical manifestation and overall recovery.