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Objective:To investigate the efficacy of tripterygium glycoside tablets combined with irbesartan for chronic nephritis and its effect on 24-hour urine protein and inflammatory factor levels.Methods:Ninety patients with chronic nephritis who received treatment at The Second People's Hospital of Liaocheng from April 2018 to January 2020 were included in this study. They were randomly divided into an observation group and a control group, with 45 patients in each group. The control group was treated with irbesartan. The observation group was treated with tripterygium glycoside tablets combined with irbesartan. All patients were treated for 3 successive months. Clinical efficacy and adverse reactions were compared between the two groups. Changes in 24-hour urine protein level, symptom score, and inflammatory factor levels after treatment relative to those before treatment were compared between the two groups.Results:Response rate in the observation group was significantly higher than that in the control group [95.6% (43/45) vs. 80.0% (36/45), χ2 = 5.07, P = 0.024). Before treatment, there were no significant differences in 24-hour urine protein level, symptom score, and inflammatory factor level between the two groups (all P > 0.05). After treatment, the 24-hour urine protein level in the observation group was significantly lower than that in the control group [(1.42±0.01) g/24 hours vs. (1.95 ± 0.05) g/24 hours, t = 69.72, P = 0.012). The symptom score in the observation group was significantly lower than that in the control group [(0.78 ± 0.01) points vs. (1.33 ± 0.12) points, t = 30.64, P = 0.001]. Serum levels of C-reactive protein, interleukin-6, and tumor necrosis factor-α in the observation group were significantly lower than those in the control group ( t = 15.70, P = 0.006; t = 96.55, P = 0.003; t = 43.41, P = 0.002). There was no significant difference in the incidence of adverse reactions between the two groups ( P = 0.694). Conclusion:Tripterygium glycoside tablets combined with irbesartan is highly effective on chronic nephritis. The combined therapy can remarkably decrease 24-hour urine protein levels, reduce symptom scores, and decrease inflammatory factor levels.
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Objective:To investigate the effect of hemodiafiltration combined with Jinshuibao tablet on serum inflammatory factors and oxidative stress indices in patients with diabetic nephropathy. Methods:A total of 86 patients with diabetic nephropathy who received treatment in The Second People's Hospital of Liaocheng from April 2019 to April 2020 were included in this study. They were randomly assigned to receive either hemodiafiltration (control group, n = 42) or hemodiafiltration combined with Jinshuibao tablet (observation group, n = 44). Microinflammatory state, oxidative stress index level, renal function and nutritional status were compared between the two groups. Results:Before treatment, serum interleukin-6, high-sensitivity C-reactive protein and tumor necrosis factor-α levels in the control group were (30.13 ± 3.25) ng/L, (9.43 ± 2.57) mg/L, (46.69 ± 3.54) ng/L respectively, and they were (30.16 ± 3.34) ng/L, (9.48 ± 2.65) mg/L, (46.73 ± 3.38) ng/L respectively in the observation group. There were no significant differences in these indices between the two groups (all P > 0.05). After treatment, serum interleukin-6, high-sensitivity C-reactive protein and tumor necrosis factor-α levels in the control group were (16.69 ± 2.73) ng/L, (8.12 ± 2.21) mg/L, (35.63 ± 2.75) ng/L, respectively, and they were (12.34 ± 2.52) ng/L, (6.47 ± 1.53) mg/L, (26.65 ± 2.13) ng/L, respectively in the observation group. After treatment, serum interleukin-6, high-sensitivity C-reactive protein and tumor necrosis factor-α levels in both groups were significantly lower than those before treatment (control group: t = 20.52, 2.50, 15.99; observation group: t = 27.60, 6.16, 32.57, all P < 0.05). After treatment, serum interleukin-6, high-sensitivity C-reactive protein and tumor necrosis factor-α levels were significantly lower than those in the control group ( t = 7.68, 4.04, 16.97, all P < 0.05). Before treatment, serum levels of malondialdehyde, superoxide dismutase, and glutathione peroxidase in the control group were (5.63 ± 1.36) nmol/L, (63.38 ± 7.56) mU/L, and (195.96 ± 26.36) IU/L, respectively, while those in the observation group were (5.68 ± 1.25) nmol/L, (63.25 ± 7.38) mU/L, and (195.83 ± 26.27) IU/L, respectively. There were no significant differences in these indices between the two groups (all P > 0.05). After treatment, serum levels of malondialdehyde, superoxide dismutase, and glutathione peroxidase in the control group were (4.83 ± 1.13) nmol/L, (83.46 ± 5.75) mU/L and (236.69 ± 18.75) IU/L respectively, while those in the observation group were (4.24 ± 0.86) nmol/L, (88.75 ± 5.47) mU/L and (258.76 ± 15.47) IU/L, respectively. After treatment, serum levels of malondialdehyde, superoxide dismutase, and glutathione peroxidase in each group were superior to those before treatment (control group: t = 2.93, 13.70, 8.16, P = 0.002, < 0.001, < 0.001; observation group: t = 6.15, 17.99, 13.37, all P < 0.001). After treatment, serum levels of malondialdehyde, superoxide dismutase, and glutathione peroxidase in the observation group were superior to those in the control group ( t = 2.73, 4.37, 5.96, P = 0.004, < 0.001, < 0.001). After treatment, blood urea nitrogen, serum creatinine and 24-hour urine protein in the observation group were significantly lower than those in the control group ( t = 7.85, 8.71, 2.06, P < 0.001, < 0.001, 0.021), and creatinine clearance rate in the observation group was significantly higher than that in the control group ( t = 3.01, P = 0.002). Total protein, prealbumin and albumin levels in the observation group were significantly higher than those in the control group ( t = 9.47, 12.13, 6.18, all P < 0.001). Conclusion:Hemodiafiltration combined with Jinshuibao tablet for the treatment of diabetic nephropathy has a positive effect on microinflammatory state and oxidative stress index level and improves patient's renal function and nutritional status.
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Objective To explore the effect and mechanism of fluvastatin on the expression of fibronectin(FN) in human peritoneal mesothelial cells (HPMCs) induced by high-glucose peritoneal dialysate (HGPDS).Methods Cultured HPMCs were randomly divided into control,HGPDS,HGPDS plus GSK650394 10-5 mol/L (the competitive inhibitor of SGK1),different concentrations of fluvastatin,fluvastatin 10-6 mol/L and GSK650394 10-5 mol/L alone.The morphology change of HPMC was observed by light microscopy.The cellular viability was detected by MTT colorimetry.The mRNA and protein expressions of serum and glucocorticoid-inducible kinase 1 (SGK1) and FN were detected by RT-PCR,Western blotting or ELISA.Results After incubation with HGPDS,the cell morphology changed from typical cobblestone-like appearance to fibroblast-like appearance,and the cell viability was inhibited significantly (P＜0.05).Fluvastatin 10-6mol/L and GSK650394 could improved the cell morphology and the cell viability injured by HGPDS (P＜0.05).Compared with the normal control group,the mRNA and protein expressions of SGK1 and FN increased significantly in HPMC treated with HGPDS(P＜0.05).GSK650394 significantly decreased the high expression of SGK1 and FN (P＜0.05),also the fluvastatin had same effects as GSK650394 in dose-dependent manner (P＜0.05).Conclusions High-glucose peritoneal dialysate can increase FN expression in human peritoneal mesothelial cells,which can be attenuated by fluvastatin.The protective role of fluvastatin in HPMC may be partially achieved through the signal pathway of SGK1.
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Objective To investigate the effect of fluvastatin (FLV) on the expression of β1 integrin in puromycin aminonucleoside (PAN)-treated podocytes and its mechanism.Methods Cultured human podocytes were divided into PAN,different concentrations of fluvastatin (1 × 10-8 to 1 × 10-5 mol/L),SOD,H2O21 groups respectively.Expressions of β1 integrin and reactive oxygen species (ROS) in podocytes were detected by Western blotting and DCFHDA (2' 7'-Dichlorofluoresecein 3' 6'-diacetate) respectively.The viability of podocyte was determined by MTT colorimetry.Results PAN and H2O2 significantly decreased the expression of β1 integrin and increased the synthesis of ROS in podocytes (P＜0.05respectively).Lower concentration fluvastatin or SOD treatment up-regulated β1 integrin and downregulated ROS of podocytes induced by PAN (P＜0.05 respectively).MTT revealed that lower podocyte viability was found in higher concentration fluvastatin,PAN and H2O2 groups.Lower concentration fluvastatin and SOD could protect podocytes against PAN.Conclusion Fluvastatin attenuates the injury of podocyte induced by PAN and increases the expression of β1 integrin,whose mechanism may be associated with the inhibition of the ROS activity.
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Objective To explore the effect and associated mechanism of fluvastatin combined with losartan on the expression of vascular endothelial growth factor (VEGF) in human podocytes induced by angiotensin (Ang)Ⅱ.Methods The differentiated human podocytes were cultured with various concentrations of Ang Ⅱ (10-9 to 10-5 mol/L) in vitro,followed by treatment of fluvastatin (10-7,10-6 and 10-5 mol/L),losartan (10-7,10-6 and 10-5 mol/L),extracellular signal-regulated kinase (ERK) inhibitor PD98059,and combination of fluvastatin and lolsartan.Expressions of VEGF and phosphorylation (p)ERK1/2 protein in podocytes were detected by Western blotting.RT-PCR was used to examine VEGF mRNA expression (P＜0.01).Results Ang Ⅱ up-regulated the expressions of VEGF and p-ERK1/2 in time-and dose-dependent manner.Above elevated expressions of VEGF and p-ERK1/2 induced by Ang Ⅱ could be down-regulated by fluvastatin,losartan and PD98059 respectively (P＜0.05).More obvious reduction of above expressions was found in combination of fluvastatin and losartan as compared to single agent (P ＜0.05).Conclusions Either fluvastatin or losartan can down-regulate the over-expression of VEGF and p-ERK1/2 induced by Ang Ⅱ in human podocytes,and their combination has a cooperative effect.The ERK signaling pathway may be one of the mechanisms of their renal protective effects.