建立了一种用离子色谱法同时测定Na_3PO_4·12H_2O中的Cl^-和SO_4^(2-)的分析方法。该方法采用分离时间20min,分离度为3.02的Metrosep A Supp 4 250/4.0型色谱柱,柱温为35℃,流速为0.8mL/min。两种离子的标准曲线的相关系数达到了0....建立了一种用离子色谱法同时测定Na_3PO_4·12H_2O中的Cl^-和SO_4^(2-)的分析方法。该方法采用分离时间20min,分离度为3.02的Metrosep A Supp 4 250/4.0型色谱柱,柱温为35℃,流速为0.8mL/min。两种离子的标准曲线的相关系数达到了0.9999。Cl^-和SO_4^(2-)的稀释液的测定结果的相对标准偏差分别为1.02%,2.26%;检出限分别为0.010mg/L,0.011mg/L;加标回收率分别96.0%,94.0%。与HG/T 2517-2009中Cl^-和SO_4^(2-)的测定方法相比,该方法的相对误差仅为分别为2.78%和0.00%。因此,该方法具有较高的精密度和准确度,且分析时间短,方法简单,可作为缓蚀阻垢剂Na_3PO_4·12H_2O中的Cl^-和SO_4^(2-)含量分析的常规方法。展开更多
目的观察豚鼠耳蜗自噬相关蛋白beclin1和LC3、Na^(+-)K^(+-)2Cl^-联合转运体(NKCC1)m RNA、内皮素(ET)表达与耳蜗庆大霉素(GM)损伤关系及盐酸椒苯酮胺(PPTA)对损伤的保护作用及其机制。方法将60只豚鼠随机分成对照组、模型组、同期治疗...目的观察豚鼠耳蜗自噬相关蛋白beclin1和LC3、Na^(+-)K^(+-)2Cl^-联合转运体(NKCC1)m RNA、内皮素(ET)表达与耳蜗庆大霉素(GM)损伤关系及盐酸椒苯酮胺(PPTA)对损伤的保护作用及其机制。方法将60只豚鼠随机分成对照组、模型组、同期治疗组、造模后对照组、后期治疗组。对照组给NS+人工外淋巴液、模型组给GM+人工外淋巴液、治疗组给GM+PPTA(均连续给药7 d),造模后对照组及后期治疗组均连续注射GM 7 d后,再分别行人工外淋巴液及PPTA连续注入7 d。所有豚鼠给药前均手术行听泡置管,NS及GM(160 mg·kg^(-1)·d^(-1))采用腹腔注射,人工外淋巴液及PPTA采用听泡注入。各组豚鼠完成给药后ABR测试分析听力,检测beclin1和LC3、NKCC1 m RNA及ET-1的表达。结果模型组、造模后对照组的ABR结果差异无统计学意义(P>0.05),但两者均明显高于其余3组(P<0.05),同期治疗组豚鼠ABR阈值明显低于后期治疗组(P<0.05);模型组LC3Ⅱ及Beclin1的表达量较其余4组明显升高,后期治疗组LC3Ⅱ及Beclin1的表达量较造模后对照组降低;模型组NKCC1 m RNA表达较其余4组明显升高(P<0.05),后期治疗组NKCC1 m RNA表达明显低于造模后对照组(P<0.05)。模型组各部位ET-1表达较其余4组明显增高,对照组各部位ET-1表达低于其余4组,后期治疗组各部位ET-1表达较造模后对照组降低。结论 PPTA可抑制耳蜗细胞自噬、NKCC1、ET-1的表达,从而对耳蜗庆大霉素损伤起到保护作用;PPTA早期对抗庆大霉素耳蜗损伤效果更优,提示GM可能对听觉细胞产生不可逆损伤。展开更多
Bumetanide has been shown to lessen cerebral edema and reduce the infarct area in the acute stage of cerebral ischemia. Few studies focus on the effects of bumetanide on neuroprotection and neurogenesis in the chronic...Bumetanide has been shown to lessen cerebral edema and reduce the infarct area in the acute stage of cerebral ischemia. Few studies focus on the effects of bumetanide on neuroprotection and neurogenesis in the chronic stage of cerebral ischemia. We established a rat model of cerebral ischemia by injecting endothelin-1 in the left cortical motor area and left corpus striatum. Seven days later, bumetanide 200 μg/kg/day was injected into the lateral ventricle for 21 consecutive days with a mini-osmotic pump. Results demonstrated that the number of neuroblasts cells and the total length of dendrites increased, escape latency reduced, and the number of platform crossings increased in the rat hippocampal dentate gyrus in the chronic stage of cerebral ischemia. These findings suggest that bumetanide promoted neural precursor cell regeneration, dendritic development and the recovery of cognitive function, and protected brain tissue in the chronic stage of ischemia.展开更多
文摘目的观察豚鼠耳蜗自噬相关蛋白beclin1和LC3、Na^(+-)K^(+-)2Cl^-联合转运体(NKCC1)m RNA、内皮素(ET)表达与耳蜗庆大霉素(GM)损伤关系及盐酸椒苯酮胺(PPTA)对损伤的保护作用及其机制。方法将60只豚鼠随机分成对照组、模型组、同期治疗组、造模后对照组、后期治疗组。对照组给NS+人工外淋巴液、模型组给GM+人工外淋巴液、治疗组给GM+PPTA(均连续给药7 d),造模后对照组及后期治疗组均连续注射GM 7 d后,再分别行人工外淋巴液及PPTA连续注入7 d。所有豚鼠给药前均手术行听泡置管,NS及GM(160 mg·kg^(-1)·d^(-1))采用腹腔注射,人工外淋巴液及PPTA采用听泡注入。各组豚鼠完成给药后ABR测试分析听力,检测beclin1和LC3、NKCC1 m RNA及ET-1的表达。结果模型组、造模后对照组的ABR结果差异无统计学意义(P>0.05),但两者均明显高于其余3组(P<0.05),同期治疗组豚鼠ABR阈值明显低于后期治疗组(P<0.05);模型组LC3Ⅱ及Beclin1的表达量较其余4组明显升高,后期治疗组LC3Ⅱ及Beclin1的表达量较造模后对照组降低;模型组NKCC1 m RNA表达较其余4组明显升高(P<0.05),后期治疗组NKCC1 m RNA表达明显低于造模后对照组(P<0.05)。模型组各部位ET-1表达较其余4组明显增高,对照组各部位ET-1表达低于其余4组,后期治疗组各部位ET-1表达较造模后对照组降低。结论 PPTA可抑制耳蜗细胞自噬、NKCC1、ET-1的表达,从而对耳蜗庆大霉素损伤起到保护作用;PPTA早期对抗庆大霉素耳蜗损伤效果更优,提示GM可能对听觉细胞产生不可逆损伤。
文摘Bumetanide has been shown to lessen cerebral edema and reduce the infarct area in the acute stage of cerebral ischemia. Few studies focus on the effects of bumetanide on neuroprotection and neurogenesis in the chronic stage of cerebral ischemia. We established a rat model of cerebral ischemia by injecting endothelin-1 in the left cortical motor area and left corpus striatum. Seven days later, bumetanide 200 μg/kg/day was injected into the lateral ventricle for 21 consecutive days with a mini-osmotic pump. Results demonstrated that the number of neuroblasts cells and the total length of dendrites increased, escape latency reduced, and the number of platform crossings increased in the rat hippocampal dentate gyrus in the chronic stage of cerebral ischemia. These findings suggest that bumetanide promoted neural precursor cell regeneration, dendritic development and the recovery of cognitive function, and protected brain tissue in the chronic stage of ischemia.
基金grants from the National Natural Science Foundation of China (No.31330037,91439205,and 81630013)National Institutes of Health of the United States (No.DK104072,HL135851, HL139689)VA Merit Review from the Department of Veterans Affairs (No.SIO1BX002817)。
