Objective To explore whether magnetotherapy is preventive in retarding diabetic kidney disease（DKD） progression and investigate underling molecular mechanisms related to its therapeutic efficacy. Methods Twenty-eigh...Objective To explore whether magnetotherapy is preventive in retarding diabetic kidney disease（DKD） progression and investigate underling molecular mechanisms related to its therapeutic efficacy. Methods Twenty-eight patients with type Ⅱ diabetes（T2D） were undergone pulsed electromagnetic fields（PEMF） stimulation at the acupoints of Píshū（脾俞 BL 20）, Zúsānl（足三里 ST 36）, Shènshū（肾俞 BL 23） and Yíshū（胰俞, EX-B3） for a period of 4 weeks. Urinary micro-albumin（U-m Alb） excretion, plasma methane dicarboxylic aldehyde（MDA and lipopolysaccharide（LPS） of the patients were used for evaluating therapeutic efficacies. Results After the acumagnetotherapy, U-m Alb excretion in the participated patients was markedly reduced（27.21±3.51 vs 8.51±0.95, P0.001） accompanied with decreased MDA（16.46±1.17 vs 12.40±1.86, P0.05） and LPS（37.41±3.84 vs 21.63±3.61, P0.05） levels in plasma while the metabolic control of these patients was not significantly altered. Acumagnetotherapy increased IκBα content（0.69±1.17 vs 1.30±0.29, P0.01）, an inhibitory protein of inflammatory response, and correspondingly reduced the protein levels of inflammatory activating proteins, NF-κB p65（0.98±0.42 vs 0.43±0.28, P0.05） and NF-κB p50（1.19±0.40 vs 0.76±0.30, P0.05）. The acumagnetotherapy also inhibited the oxidantproducing enzyme, Nox4 protein expression（1.32±0.40 vs 0.37±0.23, P0.05） in patient ＇s blood lymphocytes. Conclusion Short-term intervention of acumagnetotherapy in patients with T2 D mitigates DKD progress potentially by its anti-oxidative and anti-inflammatory effects.展开更多
目的探讨早期胰岛素治疗对2型糖尿病大鼠骨骼核因子（NF）-κB炎症信号通路的影响。方法建立高脂喂养联合小剂量链脲佐菌素诱导的2型糖尿病SD大鼠模型。糖尿病大鼠随机分为早期和晚期治疗组：早期治疗在血糖升高后3d开始，给予中效胰岛...目的探讨早期胰岛素治疗对2型糖尿病大鼠骨骼核因子（NF）-κB炎症信号通路的影响。方法建立高脂喂养联合小剂量链脲佐菌素诱导的2型糖尿病SD大鼠模型。糖尿病大鼠随机分为早期和晚期治疗组：早期治疗在血糖升高后3d开始，给予中效胰岛素或格列奇特治疗3周；晚期治疗在血糖升高后4周开始，给予中效胰岛素治疗3周。血糖控制目标是随机血糖〈8mmol／L。通过实时定量PCR和Western印迹检测骨骼肌葡萄糖转运子4（Glut4）基因和蛋白表达，胞质IκBα蛋白表达，肿瘤坏死因子（TNF）-α、白细胞介素（IL）-6、IL-1β基因表达，ELISA测定NF-κBP65DNA结合活性。结果糖尿病大鼠骨骼肌Glut4mRNA表达水平比正常对照下降59％，膜上Glut4蛋白水平下降69％。与未治疗组比较胰岛素和格列奇特治疗使Glut4mRNA表达增加了17％和13％，膜上蛋白表达增加23％和10％（0．12±0．02vs0．21±0.07和0．16±0．03，P〈0．05），并且使胞质内Glut4蛋白水平降低。糖尿病大鼠骨骼肌IKBα蛋白比正常对照降低（0．28±0．02 vs 0．36±0．06，P〈0．05）；NF-κBP65DNA结合活性增加，TNF-α、IL-1β、IL-6基因表达上调。早期胰岛素和格列奇特治疗使IKBα蛋白比未治疗组表达增加（0．41±0．06和0．39±0．05 vs 0．28±0．02，P〈0．05），NF-κBP65DNA结合活性下降，骨骼肌TNF-α基因表达下降。结论早期胰岛素治疗可抑制2型糖尿病大鼠骨骼肌细胞活化的NF-κB信号通路和炎症因子，其机制和早期代谢控制改善糖脂毒性有关。展开更多
目的:旨在提高对结外鼻型自然杀伤(natural killer,NK)细胞/T细胞淋巴瘤所致抗利尿激素分泌不当综合征(syndrome of inappropriate secretion of antidiuretic hormone,SIADH)所致稀释性低钠血症的认识。方法:报道1例结外鼻型NK细胞/T...目的:旨在提高对结外鼻型自然杀伤(natural killer,NK)细胞/T细胞淋巴瘤所致抗利尿激素分泌不当综合征(syndrome of inappropriate secretion of antidiuretic hormone,SIADH)所致稀释性低钠血症的认识。方法:报道1例结外鼻型NK细胞/T细胞淋巴瘤致顽固性低钠血症患者的临床表现及诊治过程,并结合文献进行复习。结果:患者男性,71岁,以睾丸肿大、伴多发焦痂样皮疹、顽固性低钠血症为主要临床表现。盆腔MRI检查及皮疹病理活检等排除导致低钠血症的其他相关疾病后,考虑为NK细胞/T细胞淋巴瘤(结外鼻型),且引发SIADH。该病发病率低,但疾病进展速度快,死亡率高。结论:SIADH最根本的治疗为病因治疗。对于低钠血症伴睾丸肿大和皮疹的患者,应注意NK细胞/T细胞淋巴瘤可能,及时进行病理组织活检,以避免漏诊和误诊。展开更多
基金Supported by the Natural Science Foundation of China:81270886
文摘Objective To explore whether magnetotherapy is preventive in retarding diabetic kidney disease（DKD） progression and investigate underling molecular mechanisms related to its therapeutic efficacy. Methods Twenty-eight patients with type Ⅱ diabetes（T2D） were undergone pulsed electromagnetic fields（PEMF） stimulation at the acupoints of Píshū（脾俞 BL 20）, Zúsānl（足三里 ST 36）, Shènshū（肾俞 BL 23） and Yíshū（胰俞, EX-B3） for a period of 4 weeks. Urinary micro-albumin（U-m Alb） excretion, plasma methane dicarboxylic aldehyde（MDA and lipopolysaccharide（LPS） of the patients were used for evaluating therapeutic efficacies. Results After the acumagnetotherapy, U-m Alb excretion in the participated patients was markedly reduced（27.21±3.51 vs 8.51±0.95, P0.001） accompanied with decreased MDA（16.46±1.17 vs 12.40±1.86, P0.05） and LPS（37.41±3.84 vs 21.63±3.61, P0.05） levels in plasma while the metabolic control of these patients was not significantly altered. Acumagnetotherapy increased IκBα content（0.69±1.17 vs 1.30±0.29, P0.01）, an inhibitory protein of inflammatory response, and correspondingly reduced the protein levels of inflammatory activating proteins, NF-κB p65（0.98±0.42 vs 0.43±0.28, P0.05） and NF-κB p50（1.19±0.40 vs 0.76±0.30, P0.05）. The acumagnetotherapy also inhibited the oxidantproducing enzyme, Nox4 protein expression（1.32±0.40 vs 0.37±0.23, P0.05） in patient ＇s blood lymphocytes. Conclusion Short-term intervention of acumagnetotherapy in patients with T2 D mitigates DKD progress potentially by its anti-oxidative and anti-inflammatory effects.
文摘目的探讨早期胰岛素治疗对2型糖尿病大鼠骨骼核因子（NF）-κB炎症信号通路的影响。方法建立高脂喂养联合小剂量链脲佐菌素诱导的2型糖尿病SD大鼠模型。糖尿病大鼠随机分为早期和晚期治疗组：早期治疗在血糖升高后3d开始，给予中效胰岛素或格列奇特治疗3周；晚期治疗在血糖升高后4周开始，给予中效胰岛素治疗3周。血糖控制目标是随机血糖〈8mmol／L。通过实时定量PCR和Western印迹检测骨骼肌葡萄糖转运子4（Glut4）基因和蛋白表达，胞质IκBα蛋白表达，肿瘤坏死因子（TNF）-α、白细胞介素（IL）-6、IL-1β基因表达，ELISA测定NF-κBP65DNA结合活性。结果糖尿病大鼠骨骼肌Glut4mRNA表达水平比正常对照下降59％，膜上Glut4蛋白水平下降69％。与未治疗组比较胰岛素和格列奇特治疗使Glut4mRNA表达增加了17％和13％，膜上蛋白表达增加23％和10％（0．12±0．02vs0．21±0.07和0．16±0．03，P〈0．05），并且使胞质内Glut4蛋白水平降低。糖尿病大鼠骨骼肌IKBα蛋白比正常对照降低（0．28±0．02 vs 0．36±0．06，P〈0．05）；NF-κBP65DNA结合活性增加，TNF-α、IL-1β、IL-6基因表达上调。早期胰岛素和格列奇特治疗使IKBα蛋白比未治疗组表达增加（0．41±0．06和0．39±0．05 vs 0．28±0．02，P〈0．05），NF-κBP65DNA结合活性下降，骨骼肌TNF-α基因表达下降。结论早期胰岛素治疗可抑制2型糖尿病大鼠骨骼肌细胞活化的NF-κB信号通路和炎症因子，其机制和早期代谢控制改善糖脂毒性有关。
文摘目的:旨在提高对结外鼻型自然杀伤(natural killer,NK)细胞/T细胞淋巴瘤所致抗利尿激素分泌不当综合征(syndrome of inappropriate secretion of antidiuretic hormone,SIADH)所致稀释性低钠血症的认识。方法:报道1例结外鼻型NK细胞/T细胞淋巴瘤致顽固性低钠血症患者的临床表现及诊治过程,并结合文献进行复习。结果:患者男性,71岁,以睾丸肿大、伴多发焦痂样皮疹、顽固性低钠血症为主要临床表现。盆腔MRI检查及皮疹病理活检等排除导致低钠血症的其他相关疾病后,考虑为NK细胞/T细胞淋巴瘤(结外鼻型),且引发SIADH。该病发病率低,但疾病进展速度快,死亡率高。结论:SIADH最根本的治疗为病因治疗。对于低钠血症伴睾丸肿大和皮疹的患者,应注意NK细胞/T细胞淋巴瘤可能,及时进行病理组织活检,以避免漏诊和误诊。
