The Location Of Sall1 In The Spinal Cord Of Mice And The Expression Change With SNI Model

Neuropathic pain represents a major problem in clinical medicine because it causes debilitating suffering and is largely resistant to currently available analgesics.Many studies have demonstrated a critical role of microglia in the development of neuropathic pain,the morphology,phenotype and proliferation of microglia are changed in NP.In the CNS,sall1 was restricted largely to microglia which is a transcriptional master regulator of the identity and non-reactive state of microglia and allows them to exert their housekeeping functions,which are critical for CNS homeostasis.When CNS homeostasis is disrupted by insults,including NP,the microglia rapidly move from“surveying state” into an “activated state”.Whether the expression of sall1 is changed accordingly.In this study,we established the spared nervous injury model in mice in order to explore the location and expression of sall1 in the spinal cord and future to study the possible mechanism of NP caused by peripheral nerve injury in order to provide the theoretical basis for the treatment.Objectives :Construct the neuropathic pain model of mice,and provide a good foundation to explore the the locatiaon and the expression change of sall1 in spinal cord.Methods :(1)The construction of neuropathic pain model(SNI)of mice.Neuropathic pain is induced by ligation and distally cuting off left common peroneal and tibial nerves of BALB / c mice without of the sural nerves.The paw withdrawal threshold of mice was detected by von Frey filaments to observe the change of mechanical allodynia with spared nerve injury.(2)The expression change of sall1 in L4-6 spinal cord of spared nerve injury mice at3 d,7d,10 d,14d after surgery was detected by westernblotting and Real-Time q PCR.(3)The location and IOD change of sall1 in L4-6 spinal cord of spared nerve injury mice at 3d,7d,10 d,14d after surgery were also observed by Immunohistochemistry.Results :(1)The paw withdrawal threshold of the mice with spared nerve injury was decreased From3 d after surgery until 13 d with obvious differentiation compared with the na?ve and sham operation mice(P<0.05).The most obvious decrease was at 7d and then stabilized until 13 d.(2)Western blot and Real-Time q PCR results confirmed the decrease of sall1 protein and m RNA expression in the L4-6 spinal cord induced by spared nerve injury at 3d,7d,10 d,14d with vehicle group(P< 0.05).the most significant decrease was at7 d and showed a low level of expression to 14 d.(3)The Immunohistochemistry shows that sall1 was located in the dorsal horn of L4-6 spinal cord and the IOD of sall1 in the dorsal horn of L4-6 spinal cord was decreased at 3d,7d,10 d,14d with vehicle group by Immunohistochemistry.(P< 0.05)Conclusions :(1)The mechanical hypersensitivity of mice was decreased after spared nerve injury and neuropathic pain model was successfully established.(2)The protein and m RNA expression of sall1 in the L4-6 spinal cord induced by spared nerve injury was decreased.(3)Sall1 was located in the dorsal horn of L4-6 spinal cord and IOD of sall1 was decreased after surgery.