Chronic Diseases Prevention Review (Online ISSN: 2158-0820)
Current Issue
Vol.2 No.6
Article: Effects of hyperbaric oxygen on expression of adiponectin and glucose transporter 4 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 effects of hyperbaric oxygen (HBO) on
expression adiponectin and glucose transporter 4 (GluT4) 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
increased 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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