Protective effect of berberine chloride on secondary damage of bilateral thalami in traumatic brain injury model mice

Objective To investigate the protective effect of berberine chloride on secondary damage (inflammation, oxidative damage and neuron loss) in bilateral thalami of traumatic brain injury (TBI) model mice. Methods Mice were randomly divided into 3 groups: control group (N = 6), TBI group (N = 6) and berberine group (N = 6). TBI model was established by a free-falling hitting device. In control group, mice were not given free-falling hitting. Mice in berberine group were given a gavage of berberine chloride [50 mg/（kg·d)] for 21 d, while mice in TBI group were given the same dosage of normal saline for 21 d. Immunohistochemistry was used to count the number of neurons or gliocytes positive for inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), 8-hydroxy deoxyguanosine (8-OHdG) and neuronal nuclei (NeuN), the number of astrocytes positive for glial fibrillary acidic protein (GFAP) and the number of microglias positive for ionized calcium-binding adaptor molecule 1 (Iba1).  Results The number of neurons or gliocytes positive for iNOS ( P = 0.015), COX-2 ( P = 0.022), 8-OHdG ( P = 0.000) and NeuN ( P = 0.000), the number of astrocytes positive for GFAP ( P = 0.024) and microglias positive for Iba1 ( P = 0.000) in TBI ipsilateral thalamus were significantly different among 3 groups. In TBI group, the number of neurons or gliocytes positive for iNOS ( P = 0.005), COX-2 ( P = 0.011) and 8-OHdG ( P = 0.000), the number of astrocytes positive for GFAP ( P = 0.011) and microglias positive for Iba1 ( P = 0.000) were significantly higher than those in control group, while the number of neurons positive for NeuN ( P = 0.000) was significantly lower than that in control group. In berberine group, the number of neurons or gliocytes positive for iNOS ( P = 0.031), COX-2 ( P = 0.024) and 8-OHdG ( P = 0.008), the number of astrocytes positive for GFAP ( P = 0.031) and microglias positive for Iba1 ( P = 0.012) were significantly lower than those in TBI group, while the number of neurons positive for 8-OHdG ( P = 0.014) and microglias positive for Iba1 ( P = 0.024) were significantly higher than those in control group. The number of neurons positive for NeuN in berberine group was significantly higher than that in TBI group ( P = 0.016), while lower than that in control group ( P = 0.027). Additionally, number of neurons or gliocytes positive for COX-2 ( P = 0.029) and 8-OHdG ( P = 0.000) in TBI contralateral thalamus were significantly different among 3 groups. The number of neurons or gliocytes positive for COX-2 ( P = 0.011) and 8-OHdG ( P = 0.000) in TBI group was significantly higher than that in control group, while the number of neurons or gliocytes positive for COX-2 ( P = 0.047) and 8-OHdG ( P = 0.010) in berberine group was significantly lower than that in TBI group. The number of neurons positive for 8-OHdG in berberine group was significantly higher than that in control group ( P = 0.004).  Conclusions TBI could cause secondary damage of bilateral thalami, especially in ipsilateral thalamus, but only cause inflammation and oxidative damage in contralateral thalamus. Berberine chloride might exert neuroprotective effect on bilateral thalami after TBI by significantly suppressing inflammation and oxidative damage. DOI: 10.3969/j.issn.1672-6731.2017.04.009