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1.
Chinese Journal of Geriatrics ; (12): 1314-1317, 2020.
Article in Chinese | WPRIM | ID: wpr-869572

ABSTRACT

Objective:To investigate the effects of a Baqia Huaihua Liangxue decoction on peripheral blood T helper 17 cells/Tregulatory cells(Th17/Treg)balance and the expression of related cytokines in elderly patients with psoriasis.Methods:A total of 124 elderly patients diagnosed with psoriasis and receiving treatment at our hospital from September 2018 to December 2019 were divided into the observation group and the control group according to the parity number table, with 62 cases in each group.All patients underwent conventional treatment and physical therapy, and, in addition, the observation group was treated with a Baqia Huaihua Liangxue decoction for 2 months.The blood indexes including levels of Th17, Treg, Th17/Treg, and Th17/Treg-related cytokines such as interleukin-17(IL-17), IL-22 and IL-23 in the two groups were measured before treatment and 2 months after treatment.The psoriasis area and severity index(PASI)was used to evaluate the severity of skin damage in the two groups.The traditional Chinese medicine(TCM)syndrome scores were evaluated and compared between the two groups.Adverse reactions during treatment were monitored and recorded.Results:After 2 months of treatment, the Th17 and Th17/Treg levels were lower[(1.0±0.1)% vs.(2.4±0.9)%, 0.2±0.1 vs.0.6±0.2, all P<0.05]and Treg levels were higher in the observation group than in the control group[(5.3±1.1)% vs.(4.3±1.0)%, P<0.05]. Levels of IL-17, IL-22 and IL-23 were lower in the observation group than in the control group after 2 months of treatment[(22.1±3.5)ng/L vs.(35.6±4.0)ng/L, (44.8±4.4)ng/L vs.(49.9±5.1)ng/L, (43.7±5.2)ng/L vs.(52.5±5.4)ng/L, all P<0.05]. The PASI score and TCM syndrome score were lower in the observation group than in the control group after 2 months of treatment[(2.9±1.0) vs.(6.1±2.3), (3.2±1.9) vs.(7.6±2.1), all P<0.05]. No adverse reaction occurred in the two groups during treatment. Conclusions:The Baqia Huaihua Liangxue decoction has a clear therapeutic effect in elderly patients with psoriasis.It can stabilize peripheral blood Th17/Treg balance, inhibit the expression of related cytokines, reduce the degree of skin damage and has no adverse reaction during treatment.

2.
Chinese Journal of Nephrology ; (12): 746-751, 2011.
Article in Chinese | WPRIM | ID: wpr-420072

ABSTRACT

ObjectiveTo evaluate the effects of Ang Ⅱ on apoptosis of podocytes and explore the signaling pathwayof nephrin in preventingAng Ⅱ-inducedpodocyte apoptosis.MethodsDifferentiated mouse podocytes were exposed to Ang Ⅱ at different concentrations for 18 h or at 10-8 mol/L for variable incubation times.Undifferentiated mouse pedocytes were transfected using lipofectamine 2000 with the pcDNA3.1-mNPHS1 plasmid and stably transfected cell lines were generated with G418 selection.In separated experiments,untransfected mouse podocytes (MPC) and stably transfected podocytes with pcDNA3.1-neo and PcDNA3.1-mNPHS1 were exposed toAng Ⅱ(10-8 mol/L) or LY294002(a selective Akt inhibitor,50 μmol/L) for indicated times.Apoptosis was evaluated by flow cytometry.The expression of nephrin was assessed by quantitative real-time PCR,immunofluorescence and Western blotting.The phosphorylation level of Akt was determined by Westem blotting.Results(1) AngⅡ promoted podocyte apoptosis in a dose-and time-dependentmanner. PretreatmentwithlosartansignificantlypreventedAngⅡ -induced apoptosis. (2) Nephfin mRNA and protein were obviously decreased in podocytes exposed to 10-8 mol/L Ang Ⅱ for at least 12 h than those in vehicle-treated cells (P<0.05).(3) Ang Ⅱ exposure for more than 15 min inhibited the phosphorylation of AKT in MPC,which was dramatically reversed by pcDNA3.1-mNPHS1 transfection,but not by pcDNA3.1-neo transfection. (4) Podocyte apoptosis was promoted byLY294002. Conversely,Ang Ⅱ-induced podocyteapoptosis was significantly alleviated by pcDNA3.1-mNPHS1 transfection.ConclusionAng Ⅱinduces mouse podocyte apoptosis which is suppressed by overexpression of nephrin through PI3K-Akt signaling pathway.

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