Effect of Jinmaitong (筋脉通) serum on the proliferation of rat Schwann cells cultured in high glucose medium

2008 ◽  
Vol 14 (4) ◽  
pp. 293-297 ◽  
Author(s):  
Ling Qu ◽  
Xiao-chun Liang ◽  
Hong Zhang ◽  
Qun-li Wu ◽  
Lian-qing Sun ◽  
...  
Keyword(s):  
Schwann Cells ◽  
High Glucose ◽  
Glucose Medium ◽  
High Glucose Medium ◽  
Cells Cultured

Sorbitol Accumulation In Ascorbic Acid Treated Schwann Cells Cultured In High Glucose Medium

2000 ◽  
Vol 5 (3) ◽  
pp. 183-183
Author(s):  
T Suzuki ◽  
S Yashima ◽  
K Taniko ◽  
K Mizuno ◽  
T Suzuki ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Schwann Cells ◽  
High Glucose ◽  
Glucose Medium ◽  
High Glucose Medium ◽  
Cells Cultured

scholarly journals Testosterone Protects Against Glucotoxicity-Induced Apoptosis of Pancreatic β-Cells (INS-1) and Male Mouse Pancreatic Islets

Endocrinology ◽  
2013 ◽  
Vol 154 (11) ◽  
pp. 4058-4067 ◽  
Author(s):  
Wanthanee Hanchang ◽  
Namoiy Semprasert ◽  
Thawornchai Limjindaporn ◽  
Pa-thai Yenchitsomanus ◽  
Suwattanee Kooptiwut
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
High Glucose ◽  
Male Mouse ◽  
Glucose Medium ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Stress Markers ◽  
High Glucose Medium ◽  
Cells Cultured

Male hypogonadism associates with type 2 diabetes, and T can protect pancreatic β-cells from glucotoxicity. However, the protective mechanism is still unclear. This study thus aims to examine the antiapoptotic mechanism of T in pancreatic β cells cultured in high-glucose medium. T (0.0005–2 μg/mL) was added to INS-1 cells cultured in basal glucose or high-glucose media. Then cellular apoptosis, oxidative stress, and cell viability were measured. Endoplasmic reticulum (ER) stress markers and sensors and the antiapoptotic protein (B-cell lymphoma 2) were investigated by real-time PCR and Western blot analysis. ER stress markers were also measured in male mouse pancreatic islet cultured in similar conditions. T (0.05 and 0.5 μg/mL) did not have any effect on apoptosis and viability of INS-1 cells cultured in basal glucose medium, but it could reduce apoptosis and increase viability of INS-1 cells cultured in high-glucose medium. The protective effect of T is diminished by androgen receptor inhibitor. T (0.05 μg/mL) could significantly reduce nitrotyrosine levels, mRNA, and protein levels of the ER stress markers and sensor those that were induced when INS-1 cells were cultured in high-glucose medium. It could also significantly increase the survival proteins, sarco/endoplasmic reticulum Ca2+ ATPase-2, and B-cell lymphoma 2 in INS-1 cells cultured in the same conditions. Similarly, it could reduce ER stress markers and increase sarco/endoplasmic reticulum Ca2+ ATPase protein levels in male mouse pancreatic islets cultured in high-glucose medium. T can protect against male pancreatic β-cell apoptosis from glucotoxicity via the reduction of both oxidative stress and ER stress.

scholarly journals Glucose and Prednisolone Alter Basic Fibroblast Growth Factor Expression in Peritoneal Mesothelial Cells and Fibroblasts

2001 ◽  
Vol 12 (12) ◽  
pp. 2787-2796
Author(s):  
Satoshi Ogata ◽  
Noriaki Yorioka ◽  
Nobuoki Kohno
Keyword(s):  
Growth Factor ◽  
High Glucose ◽  
Neutralizing Antibody ◽  
Mesothelial Cells ◽  
Fibroblast Growth ◽  
Glucose Medium ◽  
Peritoneal Fibrosis ◽  
Peritoneal Mesothelial Cells ◽  
High Glucose Medium ◽  
Cells Cultured

ABSTRACT. The mechanism of peritoneal fibrosis in patients on continuous ambulatory peritoneal dialysis is poorly understood. The production of basic fibroblast growth factor (bFGF) by human peritoneal mesothelial cells cultured in high glucose medium was investigated, and the behavior of peritoneal fibroblasts, as well as the inhibitory effect of prednisolone, was assessed. Reverse transcriptase-PCR and immunocytochemistry showed the expression of glucocorticoid receptors in mesothelial cells. The semiquantitative reverse transcriptase-PCR showed that high glucose medium (4.0%) increased bFGF mRNA by 2.5-fold relative to control medium (0.1% glucose), with 83% suppression of the increase by 1 μM prednisolone. The bFGF protein level in culture supernatant was also increased by 1.5-fold in high glucose medium, with this change showing 45% suppression by 1 μM prednisolone. These effects of prednisolone were prevented by a glucocorticoid receptor antagonist (RU486) in a concentration-dependent manner. The proliferation of peritoneal fibroblasts was increased 1.9-fold by the supernatant of mesothelial cells cultured in high glucose medium, with 85% suppression by 1 μM prednisolone and suppression to 16% below basal proliferation by an anti-bFGF neutralizing antibody (10 μg/ml), whereas proliferation showed a concentration-dependent increase on addition of an anti-transforming growth factor beta-neutralizing antibody. Recombinant bFGF (50 to 1000 pg/ml) likewise caused a concentration-dependent increase of peritoneal fibroblast proliferation and fibronectin release by these cells was also increased (at 50 to 5000 pg/ml). These results suggest the potential importance of bFGF for initiation of peritoneal fibrosis and the possible efficacy of glucocorticoids for preventing such fibrosis in patients receiving peritoneal dialysis.

scholarly journals Testosterone reduces AGTR1 expression to prevent β-cell and islet apoptosis from glucotoxicity

2014 ◽  
Vol 224 (3) ◽  
pp. 215-224 ◽  
Author(s):  
Suwattanee Kooptiwut ◽  
Wanthanee Hanchang ◽  
Namoiy Semprasert ◽  
Mutita Junking ◽  
Thawornchai Limjindaporn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Ang Ii ◽  
Pancreatic Β Cell ◽  
Glucose Medium ◽  
Β Cell ◽  
High Glucose Medium ◽  
Cells Cultured

Hypogonadism in men is associated with an increased incidence of type 2 diabetes. Supplementation with testosterone has been shown to protect pancreatic β-cell against apoptosis due to toxic substances including streptozotocin and high glucose. One of the pathological mechanisms of glucose-induced pancreatic β-cell apoptosis is the induction of the local rennin–angiotensin–aldosterone system (RAAS). The role of testosterone in regulation of the pancreatic RAAS is still unknown. This study aims to investigate the protective action of testosterone against glucotoxicity-induced pancreatic β-cell apoptosis via alteration of the pancreatic RAAS pathway. Rat insulinoma cell line (INS-1) cells or isolated male mouse islets were cultured in basal and high-glucose media in the presence or absence of testosterone, losartan, and angiotensin II (Ang II), then cell apoptosis, cleaved caspase 3 expression, oxidative stress, and expression of angiotensin II type 1 receptor (AGTR1) and p47phox mRNA and protein were measured. Testosterone and losartan showed similar effects in reducing pancreatic β-cell apoptosis. Testosterone significantly reduced expression of AGTR1 protein in INS-1 cells cultured in high-glucose medium or high-glucose medium with Ang II. Testosterone decreased the expression of AGTR1 and p47phox mRNA and protein in comparison with levels in cells cultured in high-glucose medium alone. Furthermore, testosterone attenuated superoxide production when co-cultured with high-glucose medium. In contrast, when cultured in basal glucose, supplementation of testosterone did not have any effect on cell apoptosis, oxidative stress, and expression of AGT1R and p47phox. In addition, high-glucose medium did not increase cleaved caspase 3 in AGTR1 knockdown experiments. Thus, our results indicated that testosterone prevents pancreatic β-cell apoptosis due to glucotoxicity through reduction of the expression of ATGR1 and its signaling pathway.

scholarly journals PTPN2 improves implant osseointegration in T2DM via inducing the dephosphorylation of ERK

2019 ◽  
Vol 244 (16) ◽  
pp. 1493-1503 ◽  
Author(s):  
Ya-Nan Wang ◽  
Tingting Jia ◽  
Jiajia Zhang ◽  
Jing Lan ◽  
Dongjiao Zhang ◽  
...  
Keyword(s):  
Osteogenic Differentiation ◽  
High Glucose ◽  
Histological Evaluation ◽  
Glucose Medium ◽  
Alizarin Red ◽  
Positive Effects ◽  
Pull Out ◽  
High Glucose Medium ◽  
Novel Target

Type 2 diabetes mellitus (T2DM) is considered to compromise implant osseointegration. Protein tyrosine phosphatase non-receptor type 2 (PTPN2) regulates glucose metabolism, systemic inflammation, and bone regeneration. This study aimed to investigate the role of PTPN2 in implant osseointegration in T2DM and explore the potential mechanisms. Streptozotocin-induced diabetic rats received implant surgery, with or without local overexpression of PTPN2 for three months, and implant osseointegration was examined by histological evaluation, micro-CT analysis, pull-out test, and scanning electron microscope. Rat bone marrow stem cells (RBMSCs) were isolated and exposed to high glucose, and osteogenic differentiation was evaluated by alizarin red staining, ALP assay, and Western blot analysis. Overexpression of PTPN2 could improve impaired implant osseointegration in T2DM rats and promote osteogenic differentiation of RBMSCs in high glucose. In addition, p-ERK level in RBMSCs was increased in high glucose and decreased after PTPN2 overexpression. These results suggest that PTPN2 promotes implant osseointegration in T2DM rats and enhances osteogenesis of RBMSCs in high glucose medium via inducing the dephosphorylation of ERK. PTPN2 may be a novel target for the therapy of impaired implant osseointegration in T2DM patients. Impact statement Using both in vivo and in vitro approaches, we made important findings that PTPN2 promoted implant osseointegration in T2DM rats and enhanced osteogenesis of RBMSCs in high glucose medium. The positive effects of PTPN2 on osteogenesis are related to the dephosphorylation of ERK and the inhibition of MAPK/ERK pathway. PTPN2 may be a novel target for the therapy of impaired implant osseointegration in T2DM patients.

Nutrient Utilization by Bovine Articular Chondrocytes: A Combined Experimental and Theoretical Approach

2005 ◽  
Vol 127 (5) ◽  
pp. 758-766 ◽  
Author(s):  
Bram G. Sengers ◽  
Hannah K. Heywood ◽  
David A. Lee ◽  
Cees W. J. Oomens ◽  
Dan L. Bader
Keyword(s):  
Oxygen Uptake ◽  
High Glucose ◽  
Articular Chondrocytes ◽  
Lactate Production ◽  
Glucose Medium ◽  
Numerical Predictions ◽  
High Glucose Medium ◽  
Biosensor System ◽  
Wide Range ◽  
Bovine Articular Chondrocytes

A combined experimental-numerical approach was adopted to characterize glucose and oxygen uptake and lactate production by bovine articular chondrocytes in a model system. For a wide range of cell concentrations, cells in agarose were supplemented with either low or high glucose medium. During an initial culture phase of 48h, oxygen was monitored noninvasively using a biosensor system. Glucose and lactate were determined by medium sampling. In order to quantify glucose and oxygen uptake, a finite element approach was adopted to describe diffusion and uptake in the experimental model. Numerical predictions of lactate, based on simple relations for cell metabolism, were found to agree well for low glucose, but not for high glucose medium. Oxygen did not play a role in either case. Given the close association between chondrocyte energy metabolism and matrix synthesis, a quantifiable prediction of utilization can present a valuable contribution in the optimization of tissue engineering conditions.

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