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Highlights: [•] The first study on serum MMP-9 and TIMP-1 expression in acute stage of acute cerebral infarction (ACI) in a rat model. [•] Our results indicate that brain edema induced by ACI is associated with increased MMP-9 response and MMP-9/TIMP-1 ratio in serum. [•] No relationship could be found between TIMP-1 and brain edema. [Copyright &y& Elsevier]

Highlights: [•] H2S is mainly formed by astrocytes and released in response to neuronal excitation. [•] H2S mediated the dilation of cerebral vessels. [•] H2S counteracts glutamate mediated excitotoxicity. [•] H2S plays the role of anti-oxidation, anti-inflammatory and anti-apoptotic effect. [•] H2S elevates intracellular Ca2+ concentration in neurons and glia. [ABSTRACT FROM AUTHOR]

Searching for effective pharmacological agents for traumatic brain injury (TBI) treatment has largely been unsuccessful. The transient receptor potential melastatin 7 (TRPM7), a TRP channel that is essential for embryonic development, has been shown to mediate ischemic neuronal injury in vivo and in vitro, but global deletion of TRPM7 in mice is lethal. Here, carvacrol was used to investigate the protective effect of TRPM7 inhibition in an in vitro traumatic neuronal injury model. Carvacrol (0.5 and 1 mM) reduced lactate dehydrogenase (LDH) release, apoptosis and caspase-3 activation after traumatic injury in cortical neurons. These neuroprotective effects were accompanied by alleviated cytoplasmic calcium levels as measured by calcium imaging. In contrast, the thapsigargin (TG) induced store-operated calcium entry (SOCE) and the expression of SOCE related proteins in neurons were not altered by carvacrol treatment. The involvement of TRPM7 sensitive calcium influx in our in vitro model was confirmed by the results that bradykinin induced calcium influx was prevented by carvacrol in neurons. Furthermore, carvacrol significantly inhibited the induction of neuronal nitric oxide synthase (nNOS) after traumatic injury, and treatment with carvacrol and the nNOS inhibitor NLPA together had no extra effect on calcium concentration and neuronal injury. Thus, inhibition of TRPM7 function by carvacrol protects against traumatic neuronal injury, and might be a potential drug development strategy for the treatment of TBI. [ABSTRACT FROM AUTHOR]

Objective To evaluate the efficacy and safety of therapeutic hypothermia in children with acute traumatic brain injury (TBI). Methods A systematic literature review using PubMed, Embase, Cochrane Library, Chinese National Knowledge Infrastructure, Wanfang, VIP, and Chinese Biomedical Database was performed to retrieve studies of randomized controlled trials (RCTs) on therapeutic hypothermia for children with TBI published before March 2014. Data extraction and quality evaluation of RCTs were performed by 2 investigators independently. A meta-analysis was performed by RevMan 5.2.7. Results There were 7 RCTs comprising 442 children (218 in hypothermia group and 224 in normothermia group). Meta-analysis showed therapeutic hypothermia could increase mortality compared with the normothermia group (relative risk [RR] = 1.84, 95% confidence interval [CI] = 1.15–2.93, P = 0.01). On the Glasgow Outcome Scale (GOS), the following scores did not differ between the hypothermia group and normothermia group: 3-month GOS 4–5 (RR = 0.89, 95% CI = 0.68–1.16, P = 0.39), 3-month GOS 1–3 (RR = 1.19, 95% CI = 0.80–1.76, P = 0.39), 6-month GOS 4–5 (RR = 0.91, 95% CI = 0.78–1.07, P = 0.26), and 6-month GOS 1–3 (RR = 1.18, 95% CI = 0.88–1.59, P = 0.27). Hypothermia did not increase the rate of pneumonia (RR = 0.84, 95% CI = 0.63–1.12, P = 0.23) or bleeding (RR = 0.94, 95% CI = 0.39–2.26, P = 0.89), but the incidence of arrhythmias was higher in the hypothermia group (RR = 2.60, 95% CI = 1.06–6.41, P = 0.04). Conclusions No benefit of therapeutic hypothermia in children with TBI is shown in this study; therapeutic hypothermia may increase the risk of mortality and arrhythmia. There is no evidence that therapeutic hypothermia improves prognosis of children with TBI; there is also no evidence that therapeutic hypothermia increases the risk of pneumonia and coagulation dysfunction. These results are limited by the quality of the included studies and need to be considered with caution. Further large-scale, well-designed RCTs on this topic are needed. [ABSTRACT FROM AUTHOR]

Highlights: [•] Allicin attenuates mechanical trauma induced neuronal injury. [•] Allicin differentially regulates NOS expression levels. [•] Allicin induced protection is dependent on NOS regulation. [•] Allicin induced regulation of NOS is mediated by Akt and ERK. [ABSTRACT FROM AUTHOR]