Chinese Journal of Tissue Engineering Research ›› 2022, Vol. 26 ›› Issue (20): 3202-3206.doi: 10.12307/2022.621

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Expression of PirB and NogoA and neurological deficits in rats with intracranial hemorrhage

Yang Yang, Liu Menglan, Meng Renliang, Tao Tao   

  1. Department of Neurology, the Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan Province, China
  • Received:2021-06-30 Accepted:2021-08-23 Online:2022-07-18 Published:2022-01-19
  • Contact: Tao Tao, MD, Associate chief physician, Department of Neurology, the Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan Province, China
  • About author:Yang Yang, Master, Physician, Department of Neurology, the Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan Province, China
  • Supported by:
    Southwest Medical University School-level Fund, No. 2017ZRQN148 (to YY)

Abstract: BACKGROUND: Neurite outgrowth inhibitor A (NogoA) and paired immunoglobulin-like receptor B (PirB) are myelin-related inhibitors and receptors. They are significantly increased in a variety of central nervous system injury models, and play a role in inhibiting axon regeneration and impeding the recovery of nerve function. Persistent and severe neurological deficits due to intracerebral hemorrhage may be related to both NogoA and PirB.
OBJECTIVE: To investigate the protein expression of PirB and NogoA and their important effect on neurological deficits by constructing a rat model of intracranial hemorrhage.
METHODS: Seventy-five male Sprague-Dawley rats were randomly assigned into a sham surgery group (n=25) and an intracranial hemorrhage group (n=50). According to the time point of sample collection, each group was randomly divided into five subgroups as a 12-hour group, a 1-day group, a 3-day group, a 7-day group, and a 14-day group. Rats in the sham surgery group did not receive any treatment, while a rat intracranial hemorrhage model was established by modified secondary injection with autologous rat tail blood in the intracranial hemorrhage group. After the neurological deficit score was performed at each time point, rats were decapitated under deep anesthesia and brain samples were taken. Western blot was used to detect the quantitative protein expression of PirB and NogoA, and the location expression of PirB was observed by immunofluorescence.
RESULTS AND CONCLUSION: PirB could be expressed in neurons and astrocytes of health adult rats. The expression of PirB and NogoA in the intracranial hemorrhage group was significantly higher than that in the sham surgery group at each time point (P < 0.05). The expression peaked on the 3rd day after intracranial hemorrhage, and remained relatively high until the 14th day. The expression of PirB and NogoA in the intracranial hemorrhage group was negatively correlated with the neurological deficit scores. These results indicate that PirB and NogoA can be both expressed in the brain tissue of health adult rats, which is significantly up-regulated and inhibits axon regeneration after intracranial hemorrhage, thereby hindering the recovery of nerve function.

Key words: intracranial hemorrhage, paired immunoglobulin-like receptor B, neurite outgrowth inhibitor A, axon regeneration, neurological deficit, rat

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