目的:探讨儿童原发性激素敏感型肾病综合征(SSNS)患儿血清25羟基维生素D_(3)[25-(OH)D_(3)]与T淋巴细胞亚群及实验室相关指标的表达水平特点及相关性。方法:选取2021年8月—2022年8月在山西省儿童医院肾内科初治的确诊为原发性肾病综合...目的:探讨儿童原发性激素敏感型肾病综合征(SSNS)患儿血清25羟基维生素D_(3)[25-(OH)D_(3)]与T淋巴细胞亚群及实验室相关指标的表达水平特点及相关性。方法:选取2021年8月—2022年8月在山西省儿童医院肾内科初治的确诊为原发性肾病综合征且经过标准剂量激素治疗4周后尿蛋白阴转的SSNS组患儿45例。同时选取同期年龄、性别相匹配的健康对照组儿童30例。比较两组儿童血清25-(OH)D_(3)、T淋巴细胞亚群、血浆白蛋白(Alb)、血脂测定[总胆固醇(TC)、三酰甘油(TG)]及24 h尿蛋白定量(24 h TPU)水平,分析25-(OH)D_(3)与T淋巴细胞亚群及实验室相关指标的相关性。结果:(1)SSNS组血清25-(OH)D_(3)、Treg细胞、CD_(3)^(+)CD_(8)^(+)(%)、Alb水平均低于健康对照组,差异有统计学意义(P<0.05);24 h TPU、TC、TG、CD_(3)^(+)CD_(4)^(+)(%)、CD_(4)^(+)/CD_(8)^(+)均高于健康对照组,差异有统计学意义(P<0.05)。(2)SSNS组中,血清25-(OH)D_(3)与Treg细胞、CD_(4)^(+)/CD_(8)^(+)、Alb水平呈正相关(β=0.335、0.458、0.343,P<0.05),与CD_(3)^(+)CD_(8)^(+)(%)、24 h TPU、TG、TC呈负相关(β=-0.437、-0.323、-0.325、-0.325,P<0.05)。结论:SSNS患儿存在25-(OH)D_(3)降低及T淋巴细胞亚群失衡,25-(OH)D_(3)与CD_(8)^(+)、CD_(4)^(+)/CD_(8)^(+)、Treg细胞、24 h TPU、Alb、血脂代谢密切相关。展开更多
旨在探究β-catenin在lα,25-(OH)2D3调控小鼠体外破骨细胞(osteoclast,OC)形成中的作用。体外诱导小鼠OC形成,添加1α,25-(OH)2D3观察其对OC形成及β-连环蛋白(β-catenin)表达的影响;敲低β-catenin进一步观察1α,25-(OH)2D3对OC形成...旨在探究β-catenin在lα,25-(OH)2D3调控小鼠体外破骨细胞(osteoclast,OC)形成中的作用。体外诱导小鼠OC形成,添加1α,25-(OH)2D3观察其对OC形成及β-连环蛋白(β-catenin)表达的影响;敲低β-catenin进一步观察1α,25-(OH)2D3对OC形成的影响。结果显示,1α,25-(OH)2D3极显著(P<0.01)抑制体外培养小鼠OC形成和骨吸收活性。敲低β-catenin,OC数量及OC形成标志物基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)蛋白和激活T-细胞核因子1(nuclear factor of activated T cells,cytoplasmic 1,Nfatc1)mRNA表达显著(P<0.05)升高。1α,25-(OH)2D3可促进OC形成过程中β-catenin基因Ctnnb1 mRNA的表达,但敲低β-catenin基因,1α,25-(OH)2D3仍可抑制OC形成。试验表明,β-catenin可抑制体外培养OC形成,但对1α,25-(OH)2D3抑制OC形成无影响。展开更多
Objective To investigate the impact of 1, 25-(OH)2D3 on left ventricular hypertrophy(LVH) in type 2 diabetic rats. Methods Type 2 diabetic mellitus(DM) model rats were established by intraperitoneally injecting with 3...Objective To investigate the impact of 1, 25-(OH)2D3 on left ventricular hypertrophy(LVH) in type 2 diabetic rats. Methods Type 2 diabetic mellitus(DM) model rats were established by intraperitoneally injecting with 30 mg/kg streptozotocin. After 8 weeks, 19 male rats were identified as diabetic with left ventricular hypertrophy(LVH) by ultrasound examination, and randomly assigned into three groups: untreated(DM-LVH, n=7), treated with insulin(DM-LVH+INS, n=6), and treated with 1, 25-(OH)2D3(DM-LVH+VD, n=6). Healthy male rats were used as the controls group(n=6). The fasting blood glucose and the insulin level were determined weekly. The left ventricular mass index, myocardial collagen content, collagen volume fraction, and 1, 25-(OH)2D3-receptor level were determined by 4 weeks later. Results In the DM-LVH model group, the insulin level was significantly decreased compared with the non-diabetic control group(P<0.05), whereas the blood glucose, left ventricular mass index, myocardial collagen content, collagen volume fraction, and 1, 25-(OH)2D3-receptor expression were significantly increased(all P<0.05). In the DM-LVH+INS and DM-LVH+VD groups, the insulin levels were significantly increased compared with the DM-LVH model group(P<0.05), whereas the other parameters were significantly decreased(all P<0.05). Conclusion 1, 25-(OH)2D3 could reverse LVH in diabetic rats and that the mechanism may involve stimulating insulin secretion and reducing blood glucose via direct up-regulation of 1, 25-(OH)2D3-receptor expression.展开更多
文摘目的:探讨儿童原发性激素敏感型肾病综合征(SSNS)患儿血清25羟基维生素D_(3)[25-(OH)D_(3)]与T淋巴细胞亚群及实验室相关指标的表达水平特点及相关性。方法:选取2021年8月—2022年8月在山西省儿童医院肾内科初治的确诊为原发性肾病综合征且经过标准剂量激素治疗4周后尿蛋白阴转的SSNS组患儿45例。同时选取同期年龄、性别相匹配的健康对照组儿童30例。比较两组儿童血清25-(OH)D_(3)、T淋巴细胞亚群、血浆白蛋白(Alb)、血脂测定[总胆固醇(TC)、三酰甘油(TG)]及24 h尿蛋白定量(24 h TPU)水平,分析25-(OH)D_(3)与T淋巴细胞亚群及实验室相关指标的相关性。结果:(1)SSNS组血清25-(OH)D_(3)、Treg细胞、CD_(3)^(+)CD_(8)^(+)(%)、Alb水平均低于健康对照组,差异有统计学意义(P<0.05);24 h TPU、TC、TG、CD_(3)^(+)CD_(4)^(+)(%)、CD_(4)^(+)/CD_(8)^(+)均高于健康对照组,差异有统计学意义(P<0.05)。(2)SSNS组中,血清25-(OH)D_(3)与Treg细胞、CD_(4)^(+)/CD_(8)^(+)、Alb水平呈正相关(β=0.335、0.458、0.343,P<0.05),与CD_(3)^(+)CD_(8)^(+)(%)、24 h TPU、TG、TC呈负相关(β=-0.437、-0.323、-0.325、-0.325,P<0.05)。结论:SSNS患儿存在25-(OH)D_(3)降低及T淋巴细胞亚群失衡,25-(OH)D_(3)与CD_(8)^(+)、CD_(4)^(+)/CD_(8)^(+)、Treg细胞、24 h TPU、Alb、血脂代谢密切相关。
文摘旨在探究β-catenin在lα,25-(OH)2D3调控小鼠体外破骨细胞(osteoclast,OC)形成中的作用。体外诱导小鼠OC形成,添加1α,25-(OH)2D3观察其对OC形成及β-连环蛋白(β-catenin)表达的影响;敲低β-catenin进一步观察1α,25-(OH)2D3对OC形成的影响。结果显示,1α,25-(OH)2D3极显著(P<0.01)抑制体外培养小鼠OC形成和骨吸收活性。敲低β-catenin,OC数量及OC形成标志物基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)蛋白和激活T-细胞核因子1(nuclear factor of activated T cells,cytoplasmic 1,Nfatc1)mRNA表达显著(P<0.05)升高。1α,25-(OH)2D3可促进OC形成过程中β-catenin基因Ctnnb1 mRNA的表达,但敲低β-catenin基因,1α,25-(OH)2D3仍可抑制OC形成。试验表明,β-catenin可抑制体外培养OC形成,但对1α,25-(OH)2D3抑制OC形成无影响。
基金Supported by the Research Fund for Public Health of the Health and Family Planning Commission of Wuhan Municipality(WG13B12)
文摘Objective To investigate the impact of 1, 25-(OH)2D3 on left ventricular hypertrophy(LVH) in type 2 diabetic rats. Methods Type 2 diabetic mellitus(DM) model rats were established by intraperitoneally injecting with 30 mg/kg streptozotocin. After 8 weeks, 19 male rats were identified as diabetic with left ventricular hypertrophy(LVH) by ultrasound examination, and randomly assigned into three groups: untreated(DM-LVH, n=7), treated with insulin(DM-LVH+INS, n=6), and treated with 1, 25-(OH)2D3(DM-LVH+VD, n=6). Healthy male rats were used as the controls group(n=6). The fasting blood glucose and the insulin level were determined weekly. The left ventricular mass index, myocardial collagen content, collagen volume fraction, and 1, 25-(OH)2D3-receptor level were determined by 4 weeks later. Results In the DM-LVH model group, the insulin level was significantly decreased compared with the non-diabetic control group(P<0.05), whereas the blood glucose, left ventricular mass index, myocardial collagen content, collagen volume fraction, and 1, 25-(OH)2D3-receptor expression were significantly increased(all P<0.05). In the DM-LVH+INS and DM-LVH+VD groups, the insulin levels were significantly increased compared with the DM-LVH model group(P<0.05), whereas the other parameters were significantly decreased(all P<0.05). Conclusion 1, 25-(OH)2D3 could reverse LVH in diabetic rats and that the mechanism may involve stimulating insulin secretion and reducing blood glucose via direct up-regulation of 1, 25-(OH)2D3-receptor expression.
