25. 3. 2018   

Chronic Diseases Prevention Review (Online ISSN: 2158-0820)


Current Issue

Vol.2  No.6


Article: Effects of hyperbaric oxygen on adiponect and glucose transporter 4 expression in type 2 diabetic rats
by  Liping Liang, Guangkai Gao, Junyu Wu
Chronic Diseases Prevention Review 2018 2(6) 1-5; published online 25 March 2018
Abstract: To investigate the effect of Hyperbaric oxygen (HBO) on adiponect and glucose transporter 4 (GluT4) expression in type 2 diabetic rats. 10 healthy control subjects (group A, n=10) were randomly selected from a total of 40 male SD rats. They were fed with normal diet. The remaining 30 rats were fed with high-fat and high sugar diet, then the model of type 2 diabetic rats was induced by intraperitoneal injection with small dose of streptozotocin (STZ). The model of type 2 diabetic rats was randomly divided into diabetic control group (group B, n=11) and diabetic hyperbaric oxygen therapy group (group C, n=10). Group C was treated with hyperbaric oxygen for 30 days. After the experiment, the serum and the specimens were obtained. Serum adiponectin, fasting insulin (FINS) and GluT4 were detected by ELISA kit. Serum high density lipoprotein (HDL-C), low density lipoprotein (LDL-C), cholesterol (TC) and triglyceride (TG) were detected with a full automatic biochemical analyzer. The expression of adiponectin receptor 2 (AdipoR2) protein in liver specimens were analysised by immunohistochemical methods. Compared with group A, fasting blood glucose(FBG), 30 minutes postprandial blood sugar, 60 minutes postprandial blood glucose, 120 minutes postprandial blood glucose, TG, TC, LDL-C, FINS, AdipoR2 in group B and group C increased significantly. HDL-C, adiponectin, Glut4 expression and insulin sensitivity decreased significantly. The difference was statistically significant (P<0.05). Group C rats were treated with hyperbaric oxygen for 30 days, then compared with group B rats: FBG, 120 minutes postprandial blood sugar, FINS,TG, AdipoR2 significantly decreased HDL-C, adiponectin, Glut4 expression and insulin sensitivity ncreased significantly. Therefore, the difference was statistically significant (P<0.05). The expression level of adiponectin and GluT4 in type 2 diabetic rats was lower than that of normal rats. Hyperbaric oxygen therapy for 30 days can improve the content of adiponectin in diabetic rats, increase the expression level of GluT4, promote the oxidation of glucose in the liver increase the uptake of glucose in the cell, lower blood sugar and improve the sensitivity of insulin.

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Article: Isatin inhibits FAK signaling pathway in neuroblastoma
by Ya’nan Hua, Shengmin Zhao, Lin Hou
Chronic Diseases Prevention Review 2018 2(6) 6-9; published online 25 March 2018
Abstract: Isatin has been shown to initiate apoptotic processes in neuroblastoma SH-SY5Y cells. Immunohistochemical (IHC) results indicated that 73% samples of neuroblastoma have detected FAK, and the phosphorylation of p125FAK increased obviously in stage IV tumors. Therefore, this study aimed to investigate whether isatin inhibited FAK signaling pathway in SH-SY5Y cells. According to the results, isatin reduced the levels of phosphorylated FAK following treatment with isatin for 48 h. In addition, isatin significantly inhibited MMP9 expression. These effects may be exerted by isatin via down-regulating the expression level of p-FAK.

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Article: Protective effect of taurine against Aβ1-40-induced toxicity
by Yuxue Liu, Lei Wang, Chuanxia Ju, Fang Zhang, zhihong Yang, Fengxiao Li, Yan Guo, Ying Yan, Xu Yao
Chronic Diseases Prevention Review 2018 2(6) 10-15; published online 25 March 2018
Abstract: In this study, we evaluated the effects of taurine against Aβ1-40 -induced neurotoxicity in vivo and in vitro experiments. Rats received an intracerebroventricular fusion of Aβ1-40 and were given taurine by intragastric administration. Then behavioral performance was assessed, which revealed that 3.2, 4.79mmol/kg taurine treatment promoted positive cognitive effects in Aβ1-40-induced rats. Further, an Aβ1-40-induced toxicity in human neuroblastoma SH-SY5Y cell model was used for investigating the mechanisms of taurine. Exposure of SH-SY5Y cells to Aβ1-40 caused cell apoptosis, reduction in cell viability and mitochondrial membrane potential (△Ψm). Pretreatment of the cells with 8, 20mmol/L taurine before Aβ1-40 exposure significantly attenuated those changes in a dose-dependent manner. These results show that taurine has significant protective effects against Aβ1-40 -induced toxicity in rats and SH-SY5Y cells, and the action mechanism may be associated with up-regulating mitochondrial membrane potential.

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Article: The exploration of modeling of rats with diabetic cardiomyopathy
by Luyan Yu, Yongjun Mao
Chronic Diseases Prevention Review 2018 2(6) 16-21; published online 25 March 2018
Abstract:  The complication of diabetic cardiomyopathy (DCM) is one of the major causes of death in diabetes mellitus (DM) patients. Accordingly, an effective animal model is playing an important role in investigating the pathogenesis of DCM. In this study, we randomized Sprague-Dawley (SD) rats into the Control group and the DCM group. The DCM rats were induced with intraperitoneal streptozotocin (STZ) injection. Eight weeks after STZ injection, compared with the Control rats, the DCM rats exhibited a series of symptoms such as polydipsia, polyphagia, polyuria, weakness, hyperglycemia and emaciation. Echocardiography results revealed that the DCM rats had a lower left ventricular ejection fraction (LVEF), fractional shortening (FS) and E wave to A wave (E/A) ratio than the Control rats. The results of hematoxylin-eosin (HE) staining showed that the left ventricle myocytes of the DCM rats were disordered and their cytoplasm was stained unevenly and their nucleus was irregular compared with the Control rats. Subsequently, as detected by transmission electron microscopy, compared with the Control rats, the apical tissue of heart displayed disorganized myofibrils and fragmented, vacuolated and swollen mitochondria in the DCM rats. Therefore, the DCM rats model were successfully induced via injecting intraperitoneally with a single STZ (65 mg/kg).

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Article: Effects of mechanosensitive ion channel Piezo1 on Osteoarthritic articular chondrocytes
by Xiaodong Li, Qing Liu, Haining Zhang 
Chronic Diseases Prevention Review 2018 2(6) 22-29; published online 25 March 2018
Abstract: Osteoarthritis (OA) is associated with abnormal mechanical stress and altering joint loads, such as obesity, trauma and joint instability, leading to joint degeneration. Abnormal mechanical stress can not only lead to joint damage in physics, but also affect the progress of OA through the baroreceptor signals. The novel stretch-activated ion channel (SACs), Piezo1, are expressed extensively in mammalian. Chondrocytes are mechano-sensation cells, so it is meaningful that Piezo1 may also exist in human OA chondrocytes and play an important role in osteoarthritis. In this research, we found that piezo1 protein was located in the cell membrane and nucleus of the OA chondrocytes. Piezo1, MMP-13, ADAMTS5 and the apoptosis-activated gene Bcl-associated X (Bax) and Bcl-2-associated death promoter (BAD) were significantly increased under mechanical stretch force and the expression was related to the degradation of Collagen II and Aggrecan. Meanwhile, the expression of the Collagen II, Aggrecan and B cell lymphoma/leukemia-2 (Bcl-2) were upregulated by GsMTx4, the specific inhibitor of Piezo1. So we got the conclusion that the Piezo1 plays an important role in human osteoarthritis, and it may be related to the degradation of extracellular matrix and the apoptosis of chondrocytes. The expression of Piezo1 protein can be inhibited by GsMTx4.

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