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In cardiovascular disorders, neurological diseases, and chronic metabolic diseases, the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway is essential for maintaining cell homeostasis. According to studies, boosting Nrf2 expression can be used to cure or prevent chronic diseases that are characterized by oxidative stress, inflammation, and mitochondrial dysfunction. Nonalcoholic fatty liver disease (NAFLD) is a chronic metabolic liver disease characterized by hepatic steatosis brought on by a number of causes other than alcohol. In recent years, its incidence has gradually risen across the globe. According to relevant studies, NAFLD and the Nrf2 signaling pathway are tightly connected. Inhibiting lipid production and metabolism-related enzymes, repairing impaired liver metabolism, and lowering hepatic lipid storage are all possible with Nrf2 activation. Exercise is a powerful tool for treating and preventing NAFLD. However, exercise type, exercise intensity, environment, and exhaustion all have an impact on the Nrf2 signaling pathway. By activating Nrf2, exercise can lessen liver inflammation, oxidative stress, endoplasmic reticulum stress, and insulin resistance, and ameliorate liver damage to improve NAFLD. The activation of Nrf2 signaling pathway, its associated mechanism of controlling antioxidation, and the impact of exercise on the Nrf2 signaling pathway are all explained in this work. Based on the pathogenesis of NAFLD, this article examines the connection between exercise, Nrf2, and NAFLD, and the current state of knowledge regarding Nrf2’s role in the amelioration of NAFLD through exercise. It offers a theoretical frame of reference for future research into how Nrf2 might be used to improve NAFLD.
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Objective To explore the changes in the serum periostin (PN) and vascular endothelial growth factor (VEGF) level in patients with diabetic retinopathy (DR) and the clinical significance.Methods The serum samples from 53 patients with diabetes mellitus (DM) as case group and 50 healthy subjects as control group were collected and compared in this study.And the DM patients included 15 patients with DM without fundus lesions (DM group),18 patients with non-proliferative diabetic retinopathy (NPDR,NPDR group) and 20 patients with proliferative diabetic retinopathy (PDR,PDR group).The serum levels of PN and VEGF were analyzed by ELISA assay,and the correlation of DR with serum PN and VEGF levels was evaluated.Results The differences in serum PN and VEGF between the case group and control group were statistically significant (both P < 0.05).And there were significant difference in PN and VEGF levels among the DM group,NPDR group,PDR group and control group (all P < 0.05).Meanwhile,there was no significant difference in serum PN between the DM group and NPDR group (P > 0.05),but there were statistically significant differences among the other groups (all P < 0.05).There were statistically significant differences in serum VEGF among the four groups (all P < 0.05).And finally,positive correlations were found between PN and VEGF in the NPDR group and PDR group (r =0.483,0.509,both P < 0.05).Conclusion PN and VEGF play an active role in the initiation and development of DR,and they have a close correlation with the neovascularization and fibrovascular membrane of the advanced stage of DR.
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This study was purpose to investigate the effects of CD147 on the invasiveness of leukemia cells U937. The experiments were divided into 4 groups: control group, LPS group, CD147mAb group and LPS+CD147 mAb group. Cells were treated by lipopolysaccharide (LPS) or anti-CD147 monoclonal antibody, and the expression of CD147 and MMP-2, -9, the invasive potential of the cells in vitro and ex vivo, as well as the invasion of the implanted tumors in SCID mice were analysed by RT-PCR, FCM, gel zymography and invasion test in vitro respectively. The results showed that the expression of CD147 was elevated by the induction of LPS, and the enhanced expression of CD147 on U937 cells increased the production and secretion of MMP-2 and MMP-9 as measured by reverse transcription-PCR and gel zymography. An increased number of LPS-induced cells invading through a reconstituted basement membrane were observed by invasion assays. These responses were down-regulated after blocking CD147 with anti-CD147 antibody. At 30 days after intravenous injection of LPS pretreated U937 cells to SCID mice human U937 cells were found in the bone marrow and lung of the mice, indicating the invasion of the tumor cells. And overexpressions of CD147, MMP-2 and MMP-9 were found in the lung tissue of the mice injected with LPS-treated but not anti-CD147 antibody treated tumor cells. It is concluded that overexpression of CD147 on U937 cells may increase the secretion and activation of MMP-2 and MMP-9 and thus promote the invasiveness of the tumor cells.
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Animais , Feminino , Humanos , Camundongos , Anticorpos Monoclonais , Farmacologia , Basigina , Genética , Alergia e Imunologia , Metabolismo , Metaloproteinase 2 da Matriz , Genética , Metabolismo , Metaloproteinase 9 da Matriz , Genética , Metabolismo , Camundongos Nus , Camundongos SCID , Invasividade Neoplásica , RNA Mensageiro , Genética , Metabolismo , Células U937RESUMO
<p><b>OBJECTIVE</b>To investigate the correlation between TCM syndrome type and intracranial aggressive potentiality of untreated nasopharyngeal carcinoma (NPC).</p><p><b>METHODS</b>Sixty untreated NPC patients of different syndrome types were treated conventionally and followed up for over one year. Correlation between the TCM syndrome type differentiated at the first consultation and the intracranial aggressive potentiality of the primary focus of NPC were analyzed.</p><p><b>RESULTS</b>The incidence of intracranial aggression was significantly higher in patients with Qi-Yin deficiency type than that in those with other two syndrome types during the follow-up period (P < 0.01).</p><p><b>CONCLUSION</b>The intracranial aggessive rate in the untreated NPC patients of Qi-Yin deficiency type was higher than in those of either Qi and blood coagulation type or fire-toxin stagnation type.</p>