Possible involvement of spinal protein kinase C in thermal allodynia and hyperalgesia in diabetic mice.
Possible involvement of spinal protein kinase C in thermal allodynia and hyperalgesia in diabetic mice.
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脊髓蛋白激酶 C 可能参与糖尿病小鼠的热异常性疼痛和痛觉过敏。
DOI：
10.1016/s0014-2999(99)00228-9
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发表时间：
1999
影响因子：
5
通讯作者：
J. Kamei
中科院分区：
文献类型：
--
作者：
M. Ohsawa;J. Kamei
我们研究了甩尾反应的各种热强度在糖尿病和非糖尿病小鼠。通过将50-W投影灯泡的源电压调节到25、35、50、65和80 V，将热强度设置为五个值之一。这些热强度分别产生0.1、0.4、0.9、3.0和7.3°C/s的表面皮肤加热速率。在35和50 V的源电压在糖尿病小鼠的甩尾潜伏期显着短于非糖尿病小鼠。然而，在25、65和80 V下，甩尾延迟没有显著差异。在非糖尿病小鼠中，鞘内（i. t.）在测试前用辣椒素预处理24小时。辣椒素预处理可增加糖尿病小鼠在35和50 V时的甩尾潜伏期。此外，虽然非糖尿病小鼠的甩尾延迟不受i.t.用选择性蛋白激酶C抑制剂calphostin C预处理，糖尿病小鼠在35和50 V下的那些增加。然而，i. t.用（8 R，9 S，11 S）-（−）-9-羟基-9-正己氧基-羰基-8-甲基-2，3，9，10-四氢-8，11-环氧-1H，8H，11 H-2，7 b，11 a-triazadibenzo [a，g]cycloocta[cde]-trinden-1-one（KT 5720）（一种选择性蛋白激酶A抑制剂）预处理，对糖尿病或非糖尿病小鼠的甩尾延迟没有影响。在非糖尿病小鼠中，i.t.用蛋白激酶C激活剂佛波醇12，13-二丁酸酯（PDB）预处理，在35和50 V下减少甩尾潜伏期。在测试前用PDB预处理60分钟。此外，i.t.在非糖尿病小鼠中用PDB预处理通过i.t.在测试前用辣椒素预处理24小时。这些结果表明，糖尿病小鼠表现出热异常性疼痛和痛觉过敏。此外，糖尿病小鼠的热异常性疼痛和痛觉过敏可能是由于脊髓中P物质的释放增加，随后蛋白激酶C的激活。
We examined the tail-flick response to various heat intensities in diabetic and non-diabetic mice. Heat intensities were set to one of five values by adjusting the source voltage of a 50-W projection bulb to 25, 35, 50, 65 and 80 V. These heat intensities produced surface skin heating rates of 0.1, 0.4, 0.9, 3.0 and 7.3°C/s, respectively. Tail-flick latencies at source voltages of 35 and 50 V in diabetic mice were significantly shorter than those in non-diabetic mice. However, there were no significant differences in tail-flick latencies at 25, 65 and 80 V. In non-diabetic mice, tail-flick latencies were not affected by intrathecal (i.t.) pretreatment with capsaicin 24 h before testing. Tail-flick latencies at 35 and 50 V in diabetic mice were increased by pretreatment with capsaicin. Moreover, although tail-flick latencies in non-diabetic mice were not affected by i.t. pretreatment with calphostin C, a selective protein kinase C inhibitor, those at 35 and 50 V in diabetic mice were increased. However, i.t. pretreatment with (8R, 9S, 11S)-(−)-9-hydroxy-9-n-hexyloxy-carbonyl-8-methyl-2, 3, 9, 10-tetrahydro-8, 11-epoxy-1H, 8H, 11H-2, 7b, 11a-triazadibenzo [a, g]cycloocta[cde]-trinden-1-one (KT5720), a selective protein kinase A inhibitor, did not affect tail-flick latencies in either diabetic or non-diabetic mice. In non-diabetic mice, i.t. pretreatment with phorbol 12,13-dibutyrate (PDB), a protein kinase C activator, decreased tail-flick latencies at 35 and 50 V. Tail-flick latencies in diabetic mice were not affected by i.t. pretreatment with PDB 60 min before testing. Furthermore, the attenuation of tail-flick latencies induced by i.t. pretreatment with PDB in non-diabetic mice was reversed by i.t. pretreatment with capsaicin 24 h before testing. These results indicate that diabetic mice exhibit thermal allodynia and hyperalgesia. Furthermore, this thermal allodynia and hyperalgesia in diabetic mice may be due to the enhanced release of substance P followed by activation of protein kinase C in the spinal cord.
影响因子：
15.9
作者：
CRAVEN, PA;DERUBERTIS, FR
通讯作者：
DERUBERTIS, FR
DOI：
10.1073/pnas.91.18.8383
发表时间：
1994-08-30
影响因子：
11.1
作者：
LIU, H;WANG, H;BASBAUM, AI
通讯作者：
BASBAUM, AI
葡萄糖水平升高引起的二酰甘油积累和微血管异常。
DOI：
10.1172/jci114988
发表时间：
1991
期刊：
The Journal of clinical investigation
影响因子：
--
作者：
Wolf,BA;Williamson,JR;Easom,RA;Chang,K;Sherman,WR;Turk,J
通讯作者：
Turk,J