Molecular neurobiology
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Molecular neurobiology · Aug 2016
Hypericum perforatum Attenuates Spinal Cord Injury-Induced Oxidative Stress and Apoptosis in the Dorsal Root Ganglion of Rats: Involvement of TRPM2 and TRPV1 Channels.
Oxidative stress and cytosolic Ca(2+) overload have important roles on apoptosis in dorsal root ganglion (DRG) neurons after spinal cord injury (SCI). Hypericum perforatum (HP) has an antioxidant property in the DRGs due to its ability to modulate NADPH oxidase and protein kinase C pathways. We aimed to investigate the protective property of HP on oxidative stress, apoptosis, and Ca(2+) entry through transient receptor potential melastatin 2 (TRPM2) and transient receptor potential vanilloid 1 (TRPV1) channels in SCI-induced DRG neurons of rats. ⋯ Mitochondria were reported to accumulate Ca(2+), provided intracellular Ca(2+) rises, thereby leading to depolarization of mitochondrial membranes and release of apoptosis-inducing factors such as caspase 3 and caspase 9. HP via regulation of NADPH oxidase and PKC inhibits TRPM2 and TRPV1 channels. The molecular pathway may be a cause of SCI-induced pain and neuronal death, and the subject should be urgently investigated.
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Molecular neurobiology · Aug 2016
Interleukin-17A Acts to Maintain Neuropathic Pain Through Activation of CaMKII/CREB Signaling in Spinal Neurons.
Immunity and neuroinflammation play major roles in neuropathic pain. Spinal interleukin (IL)-17A, as a mediator connecting innate and adaptive immunity, has been shown to be an important cytokine in neuroinflammation and acute neuropathic pain. However, the effects and underlying mechanisms of spinal IL-17A in the maintenance of neuropathic pain remain unknown. ⋯ Furthermore, we showed that blocking CaMKII with KN93 significantly reduced SNL- or rIL-17A-induced hyperalgesia and p-CREB expression. Our in vitro data showed that KN93 also significantly inhibited rIL-17A-induced CREB activation in primary cultured spinal neurons. Taken together, our study indicates that astrocytic IL-17A plays important roles in the maintenance of neuropathic pain through CaMKII/CREB signaling pathway in spinal cord, and thus targeting IL-17A may offer an attractive strategy for the treatment of chronic persistent neuropathic pain.
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Molecular neurobiology · Jul 2016
Hydrogen-Rich Saline Attenuated Subarachnoid Hemorrhage-Induced Early Brain Injury in Rats by Suppressing Inflammatory Response: Possible Involvement of NF-κB Pathway and NLRP3 Inflammasome.
Early brain injury (EBI), highlighted with inflammation and apoptosis, occurring within 72 h after subarachnoid hemorrhage (SAH), is associated with the prognosis of SAH. Recent studies have revealed that hydrogen-rich saline (HS) exerted multiple neuroprotective properties in many neurological diseases including SAH, involved to anti-oxidative and anti-apoptotic effect. We have previously reported that HS could attenuate neuronal apoptosis as well as vasospasm. ⋯ Finally, activation of NF-κB pathway and NLRP3 inflammasome contribute to the inflammation response and cellular injury in EBI after SAH. HS treatment reversed the detrimental effect mentioned above via inactivation of NF-κB pathway and NLRP3 inflammasome. NF-κB nuclear factor-κB, IκB inhibitor of NF-κB, IKK Iκ kinase, NLRP3 nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3, ASC apoptosis-associated speck-like protein containing a caspase recruitment domain.
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Molecular neurobiology · May 2016
Meta AnalysisHyperglycemia and Mortality Risk in Patients with Primary Intracerebral Hemorrhage: A Meta-Analysis.
Hyperglycemia may be associated with worse functional outcomes in patients with primary intracerebral hemorrhage. We performed a systematic review and meta-analysis to investigate the relationship between hyperglycemia and mortality risk in patients with primary intracerebral hemorrhage. We searched PubMed and Embase databases for studies investigating the association between hyperglycemia and mortality risk in patients with primary intracerebral hemorrhage. ⋯ Subgroup analysis by time of follow-up showed that hyperglycemia significantly increased risk of short-term mortality (RR = 3.97, 95% CI 2.13-7.43) and long-term mortality (RR = 1.53, 95% CI 1.14-2.05). The RR of mortality for per 1-mmol/L increment in glucose level was 1.14 (95% CI 1.06-1.22). In patients with primary intracerebral hemorrhage, hyperglycemia significantly increases risk of both short-term mortality and long-term mortality.
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Molecular neurobiology · May 2016
Plasma Homocysteine Levels Predict the Risk of Acute Cerebral Infarction in Patients with Carotid Artery Lesions.
This study examined the association between elevated plasma homocysteine (Hcy) levels and the risk of acute cerebral infarction in patients with carotid artery lesions. A total of 78 patients were divided into two groups, the high Hcy group (n = 38; Hcy levels >15 umol/L) and the low Hcy group (n = 40; Hcy levels ≤15 umol/L). High-resolution B-mode ultrasounds were performed to assess intima media thickness (IMT), infarcts, plaques, and stenosis in the extracranial carotid artery of these patients. ⋯ Pearson's test indicated that plasma Hcy levels positively correlated with IMT, total number of plaques and unstable plaques. Overall, the elevated plasma Hcy levels correlated with increased frequency of carotid plaque formation, extra- and intracranial arterial stenosis, and the degree of stenosis. In conclusion, we find a significant correlation between elevated plasma Hcy levels and the increased incidence of acute cerebral infarction in patients with carotid artery lesions.