Thioperamide treats neonatal hypoxic-ischemic encephalopathy by postsynaptic H1 receptors

Thioperamide, a selective histamine H3 receptor antagonist, can increase histamine content in the brain, improve brain edema, and exert a neuroprotective effect. This study aimed to examine the mechanism of action of thioperamide during brain edema in a rat model of neonatal hypoxic ischemic encephalopathy. Our results showed that thioperamide significantly decreased brain water content and malondialdehyde levels, while significantly increased histamine levels and superoxide dismutase activity in the hippocampus. This evidence demonstrates that thioperamide could pre vent oxidative damage and attenuate brain edema following neonatal hypoxicischemic encepha Iopathy. We further observed that changes in the above indexes occurred after combined treatment of thioperamide with the H1 receptor antagonist, pyrilamine, and the H2 receptor antagonist, ci metidine. Experimental findings indicated that pyrilamine reversed the effects of thioperamide; however, cimetidine had no significant influence on the effects of thioperamide. Our present findings suggest that thioperamide can increase brain histamine content and attenuate brain edema and oxidative damage by acting in combination with postsynaptic H1 receptors in a rat model of neo natal hypoxicischemic encephalopathy.

Effects of estrogen receptor GPR30 agonist G1 on neuronal apoptosis and microglia polarization in traumatic brain injury rats

Purpose： To investigate the effects of estrogen G protein-coupled receptor 30 （GPR30） agonist G1 on hippocampal neuronal apoptosis and microglial polarization in rat traumatic brain injury （TBI）. Methods： Male SD rats were randomly divided into sham group, TBI ＋ vehicle group, TBI ＋ G1 group. Experimental moderate TBI was induced using Feeney＇s weigh-drop method. GI （100μg/kg） or vehicle was intravenously injected from femoral vein at 30 rain post-injury. Rats were sacrificed at 24 h after injury for detection of neuronal apoptosis and microglia polarization. Neuronal apoptosis was assayed by immunofluorescent staining of active caspase-3. MI type microglia markers （iNOS and IL-113） and M2 type markers （Argl and IL-4） were examined by immunoblotting or ELLSA. Total protein level of Akt and phosphorylated Akt were assayed by immunoblotting. Results： G1 significantly reduced active caspase-3 positive neurons in hippocampus. Meanwhile G1 increased the ratio of Arg1/iNOS. IL-1β production was decreased but IL-4 was increased after G1 treatment. G1 treatment also increased the active form of Akt. Conclusions： GPR30 agonist GI inhibited neuronal apoptosis and favored microglia polarization to M2 type.

Differences in cognitive profiles between traumatic brain injury and stroke： A comparison of the Montreal Cognitive Assessment and Mini-Mental State Examination

Purpose： To investigate the profiles of cognitive impairment through Montreal Cognitive Assessment （MoCA） and Mini-Mental State Examination （MMSE） in patients with chronic traumatic brain injury （TBI） or stroke and to evaluate the sensitivity of the two scales in patients with TBI. Methods： In this cohort study, a total of 230 patients were evaluated, including TBI group （n = 103） and stroke group （n - 127）. The cognitive functions of two groups were evaluated by designated specialists using MoCA （Beijing version） and MMSE （Chinese version）. Results： Compared with the patients with stroke, the patients with TBI received significantly lower score in orientation subtest and recall subtest in both tests. MoCA abnormal rates in the TBI group and stroke group were 94.17% and 86.61% respectively, while MMSE abnormal rates were 69.90% and 57.48%, respectively. In the TBI group, 87.10% patients with normal MMSE score had abnormal MoCA score and in the stroke group, about 70.37% patients with normal MMSE score had abnormal MoCA score. The diagnostic consistency of two scales in the TBI group and the stroke group were 72% and 69%, re.spectively. Conclusion： In our rehabilitation center, patients with TBI may have mare extensive and severe cognitive impairments than patients with stroke, prominently in orientation and recall domain. In screening post- TBI cognitive impairment, MoCA tends to be more sensitive than MIV[SE.