Triggering Receptor Expressed on Myeloid Cell-2 Protects PC12 Cells Injury by Inhibiting BV2 Microglial Activation.

Microglia play a crucial role in the activation of immune defense mechanism as the resident macrophages in the central nervous system (CNS). Microglia can eliminate damaged neurons, plaques, and other infectious agents. Triggering receptor expressed on myeloid cell-2 (TREM-2) speculates to be beneficial in preventing inflammation-induced bystander damage of neurons. However, the precise molecular mechanisms underlying the regulation of TREM-2 on neurons are not clarified. We cultured PC12 cells with conditioned medium which was the supernatant of LPS-treated BV2 cells and six groups of PC12 cells (control group, LPS group, TREM-2 WT + LPS group, TREM-2 over-expression + LPS group, siRNA control + LPS group, and siRNA TREM-2 + LPS group) were investigated. The mRNA levels of inflammatory mediators: Nitric oxide synthase (iNOS) and Arginase-1(Arg-1) were quantified by using RT-PCR. Assessment of apoptosis in PC12 cells mediated by BV2 microglia was analyzed using TUNEL assays. The result showed that LPS stimulation significantly enhanced inducible iNOS (M1) production in BV2 cells (P < 0.01), and increased PC12 cells apoptosis (P < 0.01), while reduced the production of Arg-1 (M2) in BV2 cells (P < 0.01). These effects were attenuated by TREM-2 over-expression, but enhanced by TREM-2 silencing. It indicated that TREM-2 inhibited LPS-mediated neuronal apoptosis by down-regulating iNOS and up-regulating the expression of Arg-1 in BV2 microglia. Therefore, our findings may provide new insights in the regulation of TREM-2 on neuronal apoptosis via BV2 microglial M1/M2 modulation.

[Effect of transcutaneous acupoint electrical stimulation on lipid peroxidation and cognitive function in patients experiencing craniotomy].

OBJECTIVE: To observe the effect of transcutaneous acupoint electrical stimulation (TAES) on serum superoxide dismutase (SOD) activity, malondialdehyde (MDA) and S100beta contents in craniotomy patients for studying its cerebral protection mechanism. METHODS: Fifty patients scheduled for neurosurgery were randomly divided into TAES group (n = 25) and control group (n=25) with randomized block method. For patients of TAES group, TAES was applied to bilateral Hegu (LI 4) and Quchi (LI 11), Zusanli (ST 36) and Sanyinjiao (SP 6) from 30 minutes on before anesthesia to the end of operation. Patients of control group were anesthetized with sevoflurane inhalation and intermittent (i.v.) of sulfenany and vecurnium bromide. Blood samples were taken for assaying serum SOD activity, MDA and S100beta contents with purinase oxydasis, biochemiluminescence and enzyme linked immunosorbent assay separately. Scores of cognitive ability were given by using Mini Mental State Examination (MMSE). RESULTS: In comparison with pre-anesthesia, serum SOD activity decreased significantly 1 h after craniotomy in control group, at the end of operation in both control and TAES groups (P<0.05, P<0.01), and increased markedly 48 h after operation in control group (P<0.05). Serum MDA in control group increased significantly 48 h after operation, while that in TAES group reduced apparently 24 h after operation (P<0.01). Serum S100beta content in TAES group decreased remarkably 48 h after operation (P<0.01). Serum SOD activity of TAES group was significantly higher than that of control group 24 h after operation (P<0.05). Compared with control group, serum MDA contents of 24 h and 48 h after operation and serum S100beta levels at 1 h after craniotomy and 48 h after operation were markedly lower in TAES group (P<0.01, P<0.05). No significant differences were found between two groups in the cognitive function scores (P>0.05). CONCLUSION: TAES can increase serum SOD activity and reduce MDA and S100beta levels in patients undergoing craniotomy, which may contribute to its effect in reducing lipid peroxidation induced cerebral injury. But its impact on the patient's cognitive function needs study further.

[Effect of transcutaneous acupoint electrical stimulation on blood bioactive compounds involving cerebral injury during craniotomy].

OBJECTIVE: To observe the effect of transcutaneous acupoint electrical stimulation (TAES) on plasma ET, CGRP and serum IL-6, S100beta during craniotomy. METHODS: Fifty patients scheduled for neurosurgery were randomly divided into TAES group (n=25) and control group (n=25). TAES (2/100 Hz, 8-12 mA) of bilateral Hegu (LI 4)-Quchi (LI 11), Zusanli (ST 36)-Sanyinjiao (SP 6) was administrated for patients of TAES group starting 30 min before anesthesia till the end of the operation. Anesthesia of the patients was maintained with sevoflurane inhalation and intermittent intravenous injection of boluses of sulfenany and vecurnium bromide. Jugular venous blood samples were taken at preanesthesia (T0), 1 hour after craniotomy (T1), closure complete (T2), 24 hours (T3) and 48 hours (T4) after operation respectively for detecting contents of plasma endothelin (ET), calcitonin gene-related peptide (CGRP) and serum interleukin (IL)-6, S100beta with radioimmunoassay and enzyme linked immunosorbent assay separately. RESULTS: Compared with control group, plasma ET at T2, serum IL-6 at T1 S100beta at T1 and T4 in TAES group all decreased significantly (P < 0.01, 0.05), while serum IL-6 at T3 increased remarkably (P < 0.05). It suggests that after TAES, CGRP/ET was improved, favoring cerebral microcirculation to reduce surgery-induced cerebral injury. There were no significant differences between two groups at different time courses in plasma CGRP concentrations (P > 0.05). CONCLUSION: TAES can regulate plasma CGRP/ET and serum IL-6, lower serum S100beta level, which may contribute to its effect in relieving craniotomy-induced brain injury.