ABSTRACT
[Summary] The HK-2 cells with different culture media were divided into normal glucose group (NG group,5.5 mmol/L D-glucose) ; high glucose group (HG group,30 mmol/L D-glucose) ; mannitol group (MG group,5.5mmol/L D-glucose+24.5 mmol/L mannitol) ; 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] groups (V1-V3 group)which were exposed to medium containing 30 mmol/L D-glucose and different concentrations of 1,25-(OH)2D3 ;Nethyl-cysteim control group (NAC group,30 mmoL/L D-glucose + 1.0 mmol/L N-Nethyl-cysteim) ; and ethanol control group(SG group,30 mmol/L D-glucose+6.86 × 10-2 mol/L ethanol).The level of intracellular reactive oxygen species,mitochondrial membrane potential,activity of total-superoxide dismutase (T-SOD),level of malondialdehyde,expression of UCP2 mRNA and protein in HK-2 cells were detected.Compared with NG group,the mitochondrial membrane potential significantly decreased in HG group (P＜0.01),and the mitochondrial membrane potential in V group was lower than that in HG group(P＜0.01).The activity ofT-SOD in HG group was significantly lower than that in NG group(P＜0.01),while its level of malondialdehyde was significantly higher than that in NG group(P＜0.01).Compared with HG group,the activity of T-SOD in V groups was significantly increased (P＜0.05)and the level of malondialdehyde in these groups significantly decreased (P＜0.01).The mRNA expression of UCP2 in HG group was increased significantly in comparison with NG group (P ＜ 0.05) and the expression in V groups was significantly decreased in comparison with HG group (P＜0.01).The results suggest that 1,25-(OH)2D3 could reduce the mitochondrial membrane potential,the production of reactive oxygen species,and regulate the expression of UCP2 in order to suppress the oxidative stress induced by high glucose.
ABSTRACT
HK-2 cells cultured in vitro were divided into three groups: normal glucose group ( NG ), high glucose group( HG), and mannitol group(MG). The expression of angiotensin-converting enzyme( ACE ) and ACE2 mRNA in HK-2 cells was detected. The concentration of angiotensin Ⅱ ( Ang Ⅱ ) in the culture medium was detected. The mRNA and protein expression of ACE and ACE2 existed in normal cultured HK-2 ( NG group ). In comparison with NG group, the mRNA and protein expressions of ACE in HG group increased significantly ( P＜0. 01 ), and the expression of ACE2 mRNA decreased significantly( P＜0. 01 ). The level of Ang Ⅱ in HG group was significantly higher than in NG group( P＜0. 05 ). The result show that high glucose may induce ACE expression and inhibit ACE2 expression, then promote synthesis of Ang Ⅱ in proximal tubular cells.
ABSTRACT
Objective To investigate the effects of benazepril on urinary excretion of endothelin 1(Et 1) and the level of plasmic Et 1 (PEt) in patients with diabetes mellitus (DM) and diabetic nephropathy(DN).Methods PEt and 24 hours urinary excretion of Et 1 (UEtV) in 54 patients with DM and 39 patients with DN before and after taking benazepril (7.5～12.5mg/d) for two months were measured using radioimmunoassay method.Results PEt and UEtV in patients with DM were significantly higher than in normal control group ( P
ABSTRACT
AIM: To investigate the effect of interleukin-13 (IL-13) on cell proliferation and interleukin-6 (IL-6) production in mesangial cells. METHODS: Cell proliferation was tested by MTT method. The protein synthesis of IL-6 in mesangial cells was measured by ELISA. The expression of IL-6 mRNA in mesangial cells was evaluated by RT-PCR. RESULTS: IL-13(1 ?g/L-100 ?g/L) inhibited the proliferation of mesangial cell in a dose-dependent manner. Both mRNA and protein of IL-6 in mesangial cells were increased significantly in the presence of LPS and this increase could be reversed by IL-13 (1?g/L-100?g/L). However, this increase could not be reversed by IL-13 if the dose was lower than 0.1?g/L and if the mesangial cells were cultured in 5% FCS RPMI1640. CONCLUSION: IL-13 could inhibit IL-6 expression induced by LPS in mesangial cells . We suggested that IL-13 may be an inhibitory cytokine in the regulation of the mesangial cell proliferaltion and inflammatory reaction in glomerulonephritis.