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Objective: This study aimed to investigate the effect and mechanism of Liraglutide on high glucose-induced vascular endothelial cell injury. Methods Human umbilical vein endothelial cells (HUVECs) were cultured and divided into 4 groups: control, high glucose stimulation (HG), Liraglutide, and Liraglutide + HG group. ELISA was used to detect the secretion of inflammatory cytokines in each group, kits the levels of intracellular reactive oxygen species (ROS), the activity of SOD2 and Gpx4,and the level of MDA, and Western blot and immun of luorescence method nuclear translocation of Nrf2. Results The HG groupexhibited a significantly higher levels of tumor necrosis factor (TNF-α), interleukin (IL-1), IL-6, as well as the levels of intracellular ROS and MDA, but less activity of SOD2 and Gpx4, less contents of NO, and less nuclear translocation of Nrf2, as compared with the control group. Compared with the HG group, the Liraglutide + HG grouppresented significantly higher levels of TNF-α, IL-1, and IL-6, but lower levels of intracellular ROS and MDA, less activities of SOD2 and Gpx4, less contents of NO and less nuclear translocation of Nrf2. Conclusion Liraglutide suppresses high glucose-induced endothelial cell injury by increasing the nuclear translocation of Nrf2. [ABSTRACT FROM AUTHOR]

Classic of Changes is a Chinese cultural classic born more than 3000 years ago. Its profound philosophical thoughts and the use of divination have brought Classic of Changes to a strong oriental mysticism. The view of the heaven and man of yin and yang and the five elements states of Classic of Changes are completely different from the Western elemental theory of ancient Greece. The latter gave birth to classical and modern scientific theories, and the yin and yang and the eight trigrams symbol has become synonymous with oriental mysticism. In fact, the cosmology of the Holism of Classic of Changes is a precious scientific heritage of mankind. The axiomatization of the symbolic formal system of Classic of Changes aims to unveil the veil of oriental mysticism and provide oriental wisdom for the development of modern science. Transforming the symbolic system of Classic of Changes into a formal axiom system is the crystallization of the fusion of wisdom between the East and the West. The axiomatization of the symbolic formal system of Classic of Changes shows that the oriental and the western scientific tradition harmony but not sameness and there is no conflict. Classic of Changes can also be interpreted by the axiomatic system like Euclid's Elements. The main contribution of this paper is that the author skillfully uses mathematical language to formulate the system of Classic of Changes, reconstructs the ideological system of Classic of Changes with the axiomatic method and realizes the scientificalization of Chinese classical natural philosophy. The formal axiom system of Classic of Changes may give us such a revelation: the gap between the oriental and western scientific traditions is mainly in the axiomatization, but the lack of oriental scientific tradition may be the bottleneck of the development of modern science., Author(s): Xijia Wang [sup.1] Author Affiliations: (1) grid.411427.5, 0000 0001 0089 3695, College of Mathematics and Statistics, Hunan Normal University, , 410081, Changsha, China Introduction Formalization and axiomatization are the [...]

Background and purpose: To investigate the effect of Emodin on the inflammatory response of brain tissue and the expression of the TLR3 pathway in mice with herpes virus encephalitis. Method: Twenty male BALB/c mice were randomly divided into the NS group, HSV-1 group, HSV-1 + Emodin group and HSV-1 + ACV group. The histopathological features and the effect of TLR3 expression were observed by staining and immunohistochemistry (IHC) respectively. The gene expression of TLR3, trif, TRADD, TRAF6, traf3, p38, Nemo and IRF3 was detected by polymerase chain reaction (PCR). The protein production of TLR3 and its downstream molecules was detected by Western blot. The expression of IL-6, TNF-α and IFN-β in the brain tissues was detected by ELISA. Result: Compared to the HSV-1 group, the pathological changes (inflammatory cell infiltration, necrotic temporal lobe and massive hemorrhage) were not as obvious as those in the HSV-1+emodin and HSV-1+ACV groups. The TLR3 staining increased significantly in the HSV-1 groups and decreased in the HSV-1 + emodin group. Compared with the NS group, the mRNA expression of TLR3, TRIF, TRADD, TRAF6, traf3, p38, NEMO and IRF3 decreased by 20%–60% in the HSV-1 + emodin group and 30% in the HSV-1 + ACV group, respectively. The expression of IL-6, TNF-α and IFN-β decreased by 30%-50% in the HSV-1 + emodin group and showed no significant change in the HSV-1 + ACV group, respectively. Conclusion: Emodin could inhibit the inflammatory response in the brain of mice with herpes virus encephalitis. The inhibition of TLR3 expression may play an important role in this process. [ABSTRACT FROM AUTHOR]

TIM‐4 plays an important role in ischaemia‐reperfusion injury of liver and kidney; however, the effects of TIM‐4 on cerebral ischaemia‐reperfusion injury (IRI) are unknown. The purpose of the present study was to investigate the potential role of TIM‐4 in experimental brain ischaemia‐reperfusion injury. In this study, cerebral ischaemia reperfusion was induced by transient middle cerebral artery occlusion (MCAO) for 1 hour in C57/BL6 mice. The TIM‐4 expression was detected in vivo or vitro by real‐time quantitative polymerase chain reaction, Western blot and flow cytometric analysis. In vivo, the administration of anti‐TIM‐4 antibodies significantly suppressed apoptosis, inhibited inflammatory cells and enhanced anti‐inflammatory responses. In vitro, activated microglia exhibited reduced cellular proliferation and induced IRI injury when co‐cultured with neurons; these effects were inhibited by anti‐TIM‐4 antibody treatment. Similarly, microglia transfected with TIM‐4 siRNA and stimulated by LPS + IFN‐γ alleviated the TIM‐4‐mediated damage to neurons. Collectively, our data indicate that the inhibition of TIM‐4 can improve the inflammatory response and exerts a protective effect in cerebral ischaemia‐reperfusion injury. [ABSTRACT FROM AUTHOR]

Adipose dysfunction in lipodystrophic SEIPIN deficiency is associated with multiple metabolic disorders and increased risks of developing cardiovascular diseases, such as atherosclerosis, cardiac hypertrophy, and heart failure. Recently, adipose transplantation has been found to correct adipose dysfunction and metabolic disorders in lipodystrophic Seipin knockout mice; however, whether adipose transplantation could improve lipodystrophy-associated cardiovascular consequences is still unclear. Here, we aimed to explore the effects of adipose transplantation on lipodystrophy-associated metabolic cardiovascular diseases in Seipin knockout mice crossed into atherosclerosis-prone apolipoprotein E ( Apoe ) knockout background. At 2 months of age, lipodystrophic Seipin/Apoe double knockout mice and nonlipodystrophic Apoe knockout controls were subjected to adipose transplantation or sham operation. Seven months later, mice were euthanized. Our data showed that although adipose transplantation had no significant impact on endogenous adipose atrophy or gene expression, it remarkably increased plasma leptin but not adiponectin concentration in Seipin/Apoe double knockout mice. This led to significantly reduced hyperlipidemia, hepatic steatosis, and insulin resistance in Seipin/Apoe double knockout mice. Consequently, atherosclerosis burden, intraplaque macrophage infiltration, and aortic inflammatory gene expression were all attenuated in Seipin/Apoe double knockout mice with adipose transplantation. However, adipocyte morphology, macrophage infiltration, or fibrosis of the perivascular adipose tissue was not altered in Seipin/Apoe double knockout mice with adipose transplantation, followed by no significant improvement of vasoconstriction or relaxation. In conclusion, we demonstrate that adipose transplantation could alleviate lipodystrophy-associated metabolic disorders and atherosclerosis but has an almost null impact on perivascular adipose abnormality or vascular dysfunction in lipodystrophic Seipin/Apoe double knockout mice. NEW & NOTEWORTHY Adipose transplantation (AT) reverses multiply metabolic derangements in lipodystrophy, but whether it could improve lipodystrophy-related cardiovascular consequences is unknown. Here, using Seipin/Apoe double knockout mice as a lipodystrophy disease model, we showed that AT partially restored adipose functionality, which translated into significantly reduced atherosclerosis. However, AT was incapable of reversing perivascular adipose abnormality or vascular dysfunction. The current study provides preliminary experimental evidence on the therapeutic potential of AT on lipodystrophy-related metabolic cardiovascular diseases.