We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
The effect and regulation mechanism of TRPC channels in delayed neuronal apoptosis after subarachnoid hemorrhage in rats.
- Authors
GUO Xiao-ye; SONG Jin-ning; ZHANG Ming; ZHAO Yong-lin; LI Dan-dong; FU Zhou-feng; PANG Hong-gang
- Abstract
Objective To investigate the possible role of canonical trasnient receptor potential channels (TRPCs) in calcium overload of neurons after subarachnoid hemorrhage (SAH) and discuss the mechanism of TRPCs involved in delayed neuronal death (DND) after SAH. Methods Rat models of SAH were established by double-blood injection via the citerna magna. SAH intervention group was established by using SKF96365 intracerebroventricular injection. Intracellular calcium concentration was detected by Fura-2AM. The dynamic expressions of TRPCs in the cortex and basilar artery were determined by Western blot. The mRNA levels of TRPCs in the cortex and basilar artery were determined by RT-PCR. The results were compared with those in DMSO control model group, saline control group and normal group. The apoptosis of cortical neurons was detected by TUNEL. One-way ANOVA was used to compare within each group. Results The protein expressions and mRNA levels of TRPC1 in the cortex and the basilar artery continuourly increased after SAH and reached the peak on day 5 while intracellular calcium concentration and TUNEL-positive cell counts also reached the peak. After injection of SKF96365, a TRPCs blocker, the protein expressions and mRNA levels of TRPC1 were inhibited, intracellular calcium concentration and TUNEL-positive cell counts decreased. Meanwhile, the scores of rat neurological functions were improved. The expressions of TRPC3 in the cortex and the basilar artery showed no significant change. Conclusion TRPC1 induced calcium overload and CVS after SAH are the major causes of delayed neuronal death. Suppressing calcium influx induced by TRPC1 could delay neuronal death and improve neurological functions.
- Subjects
NEURAL physiology; APOPTOSIS; LABORATORY rats; BRAIN injuries; MESSENGER RNA; CALCIUM channels
- Publication
Journal of Xi'an Jiaotong University (Medical Sciences), 2013, Vol 34, Issue 6, p728
- ISSN
1671-8259
- Publication type
Article
- DOI
10.7652/jdyxb201306006