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#28962173   2017/09/30 Save this To Up

Tetramethylpyrazine reduces blood-brain barrier permeability associated with enhancement of peripheral cholinergic anti-inflammatory effects for treating traumatic brain injury.

Traumatic brain injury (TBI) is a diverse group of intracranial injuries resulting from external mechanical insults to the brain. While basic and clinical research for TBI has been conducted for decades, it has not identified cost-effective medical interventions for treating TBI. Tetramethylpyrazine (TMP), which is derived from the Chinese herb, Ligusticum chuanxiong Hort (Chuan Xiong), has been clinically used for treating ischemic brain injury for years. However, whether TMP could provide effective benefits for improving the outcomes following TBI is unknown. In the present study, using controlled cortical impact (CCI) injury to create an animal model of TBI, the potential effects of TMP on improving blood-brain barrier (BBB) permeability in the early phase of the secondary injury, as well as the splenic anti-inflammatory activities, were evaluated. Cognitive functions were also assessed by Morris water maze trials following TBI. Results demonstrated that, at 24 h after CCI injury, BBB permeability was significantly reduced (P<0.05) by the application of TMP. In addition, within 24 h after CCI injury, the plasma levels of interleukin (IL)-1β and tumor necrosis factor (TNF)-α, and protein and mRNA expression levels of IL-1β and TNF-α in the spleen were significantly lowered by TMP (P<0.05). Furthermore, within 24 h after CCI injury, the activation of the splenic anti-inflammatory effects mediated by nicotinic acetylcholine receptor α7 (nAChRa7) stimulation were significantly enhanced by TMP (P<0.05). Additionally, impaired spatial memory acquisition and consolidation were significantly improved by TMP after CCI injury (P<0.05). Together, in light of these data, in the treatment of TBI, TMP could effectively reduce BBB permeability, which may be closely associated with the enhanced splenic anti-inflammatory effects activated by nAChRa7 stimulation, and potentially improve cognitive recovery concerning spatial learning and memory.

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#28950359   2017/09/26 Save this To Up

Recipient treatment with acetylcholinesterase inhibitor donepezil attenuates primary graft failure in rats through inhibiting post-transplantational donor heart ischaemia/reperfusion injury.

Ischaemia/reperfusion injury may have deleterious consequences on heart transplantation. The underlying causes such as inflammation may also contribute to the pathogenesis of primary or chronic graft failure. We hypothesize that donepezil (DO), a reversible acetylcholinesterase inhibitor that increases cholinergic receptor activation, may protect the transplanted heart through increasing the level of acetylcholine, which in turn inhibits systemic inflammation in the recipients.

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#28944927   2017/09/25 Save this To Up

α7 nicotinic acetylcholine receptor agonist attenuates the cerebral injury in a rat model of cardiopulmonary bypass by activating the Akt/GSK3β pathway.

α7 nicotinic acetylcholine receptor (α7nAchR) agonist treatment may provide a promising therapeutic effect for cerebral injuries. However, it is unclear whether the activation of α7nAchR agonist may reduce cerebral injuries induced by cardiopulmonary bypass (CPB). A total of 96 male Sprague‑Dawley rats were randomly divided into four groups (n=24/group): i) Sham operation group; ii) CPB group; iii) CPB + α7nAchR agonist group; and iv) CPB + α7nAchR agonist + α7nAchR antagonist group. Following treatment, 24 rats from each group were sacrificed and the serum and hippocampal tissues were collected. The serum expression levels of S100β, interleukin 6 and tumor necrosis factor α were evaluated by ELISA, hippocampal tissues were analyzed by histopathological examination using hematoxylin & eosin and terminal deoxynucleotidyl‑transferase‑mediated dUTP nick‑end labeling (TUNEL) staining and Caspase 3 expression in the hippocampal tissues was evaluated by immunohistochemistry. In addition, Caspase 3, Akt and glycogen synthase kinase 3β (GSK3β), as well as phosphorylated (p)‑Akt and (p)‑GSK3β were examined by western blot assay. The present study demonstrated that α7nAchR agonist treatment was able to alleviate pathological damage and inhibit hippocampal cell apoptosis and inflammatory response. α7nAchR agonist treatment also increased the expression levels of p‑Akt and p‑GSK3β, which indicated an upregulation in Akt/GSK3β signaling. These data suggested that α7nAchR agonist may provide a promising new therapeutic approach for cerebral injury caused by CPB.

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#28883881   2017/09/08 Save this To Up

Zinc and Copper Metabolism and Risk of Autism: a reply to Sayehmiri et al.

Sayehmiri et al. recently conducted a meta-analysis to explore the relationship between zinc and copper metabolism and autism spectrum disorders (ASD). Recent reports have elucidated a full behavioral profile of mice exposed to prenatal zinc deficiency and documented a phenotype similar to that found in autism spectrum disorders (ASD). These studies suggest that significant alterations in Zn metabolism may be an important nutritional component in the development of ASD.

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#28878016   2017/09/07 Save this To Up

Enantiomeric barbiturates bind distinct inter- and intrasubunit binding sites in a nicotinic acetylcholine receptor (nAChR).

Nicotinic acetylcholine receptors (nAChRs) and γ-aminobutyric acid type A receptors (GABAARs) are members of the pentameric ligand-gated ion channel superfamily. Drugs acting as positive allosteric modulators of muscle-type α2βγδ nAChRs, of use in treatment of neuromuscular disorders, have been hard to identify. However, identification of nAChR allosteric modulator binding sites has been facilitated by using drugs developed as photoreactive GABAAR modulators. Recently, R-1-methyl-5-allyl-5-(m-trifluoromethyl-diazirinylphenyl) barbituric acid (R-mTFD-MPAB), an anesthetic and GABAAR potentiator, has been shown to inhibit Torpedo α2βγδ nAChRs, binding in the ion channel and to a γ(+)-α(-) subunit interface site similar to its GABAAR intersubunit binding site. In contrast, S-1-methyl-5-propyl-5-(m-trifluoromethyl-diazirinylphenyl) barbituric acid (S-mTFD-MPPB) acts as a convulsant and GABAAR inhibitor. Photolabeling studies established that S-mTFD-MPPB binds to the same GABAAR intersubunit binding site as R-mTFD-MPAB, but with negative rather than positive energetic coupling to GABA binding. We now show that S-mTFD-MPPB binds with the same state (agonist) dependence as R-mTFD-MPAB within the nAChR ion channel, but it does not bind to the intersubunit binding site. Rather, S-mTFD-MPPB binds to intrasubunit sites within the α and δ subunits, photolabeling αVal-218 (αM1), δPhe-232 (δM1), δThr-274 (δM2), and δIle-288 (δM3). Propofol, a general anesthetic that binds to GABAAR intersubunit sites, inhibited [(3)H]S-mTFD-MPPB photolabeling of these nAChR intrasubunit binding sites. These results demonstrate that in an nAChR, the subtle difference in structure between S-mTFD-MPPB and R-mTFD-MPAB (chirality; 5-propyl versus 5-allyl) determines selectivity for intra- versus intersubunit sites, in contrast to GABAARs, where this difference affects state dependence of binding to a common site.

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#28867899   2017/09/04 Save this To Up

Homology Modeling and Protein Interaction Map of CHRNA7 Neurogenesis Protein.

CHRNA7 is a neurodevelopmental protein involved in differentiation and neurogenesis, which is also named as nicotinic acetylcholine receptors, cholinergic receptor, nicotinic, alpha 7 (neuronal). The protein encoded by this gene forms a homo-oligomeric channel. It is a major component of brain nicotinic receptors displays that are blocked by and sensitive to alpha-bungarotoxin. Studies reports involvement of CHRNA7 protein in different neurological diseases. Non-availability of 3-dimensional (3D) structure leads the study toward structure 3D prediction along with its interaction analysis. The current paper is focused on the structure prediction through homology modeling of CHRNA7 along with binding site prediction using Schrödinger software suite. In continuation of the study, protein-protein interaction analysis is carried out by using string database. Tertiary structure along with binding sites was obtained, and visualized CHRAN7 protein have interaction with CHRNA protein family along with JAK2, AKT1, PICK1 protein that are involved in neurological disease. Structure formation analysis is an important aspect of proteomics studies. Hence, this predicted structure can be used for further advance studies and drug designing. Protein interaction analysis shows that CHRNA7 protein also interact with AKT1 protein which regulate neuronal differentiation and development, that signifies the role of CHRNA7 protein in neurological diseases.

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#28858686   2017/08/31 Save this To Up

Nicotinic acetylcholine receptor alpha 7 stimulation dampens splenic myelopoiesis and inhibits atherogenesis in Apoe(-/-) mice.

Monocyte levels predict cardiovascular outcomes and play a causal role in atherogenesis. Monocytes can be produced in the spleen and track to the atherosclerotic lesion in significant numbers. The cholinergic system has been shown to have anti-inflammatory actions in the spleen. We aimed to explore whether therapeutic stimulation of the nicotinic acetylcholine receptor alpha 7 (nAChRα7) can suppress atherogenesis.

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#28842280   2017/08/26 Save this To Up

Electroacupuncture alleviates surgery-induced cognitive dysfunction by increasing α7-nAChR expression and inhibiting inflammatory pathway in aged rats.

Postoperative cognitive dysfunction (POCD) is a common disorder of cognitive functions in aged patients following anesthesia and surgery. α7-nicotinic acetylcholine receptors (α7-nAChR) plays a regulatory role in cognitive processes and is involved in cognitive deficits. This study aims to observe the effect of electroacupuncture (EA) on the cognitive function in aged POCD rats, and its regulation on expressions of hippocampal α7-nAChR and proinflammatory factors. Ninety healthy Sprague-Dawley male aged rats were randomly divided into three groups (each n=30): control group (sham operation), model group (partial hepatectomy), and electroacupuncture (EA) group. The cognitive function was detected by Morris water-maze test, and the changes of hippocampal expressions of α7-nAChR, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were detected by immunohistochemical method. Our results showed that compared with the model group, the EA group had significantly shorter escape latency and decreased crossing platform times at 1d, 3d and 7d after operation (P<0.05). α7-nAChR positive neurons in the hippocampus decreased and TNF-α and IL-1β positive neurons increased on postoperative days 1, 3 and 7. Compared with the model group, the α7-nAChR positive neurons were increased and TNF-α and IL-1β positive neurons were decreased in the EA group at the same time points (P<0.05). In conclusion, the electroacupuncture regulation can improve the learning and memory abilities in POCD rats, and its mechanism may be related to upregulation of α7-nAChR and downregulation of TNF-α and IL-1β in hippocampus.

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#28800036   2017/08/11 Save this To Up

Improved Outcomes of Cardiopulmonary Resuscitation in Rats Treated with Vagus Nerve Stimulation and its Potential Mechanism.

Studies have demonstrated that vagus nerve stimulation (VNS) reduces ischemia/reperfusion (I/R) injury. In this study, we investigated the protective effects of VNS in a rat model of cardiopulmonary resuscitation (CPR). We further investigated whether the beneficial effects of VNS were dependent on the alpha 7 nicotinic acetylcholine receptor (α7nAChR). Forty animals were randomized into 4 groups and all underwent CPR (n = 10 each): (1) CPR alone (control); (2) VNS during CPR; (3) α7nAChR antagonist methyllycaconitine citrate (MLA) with VNS; (4) α7nAChR agonist 3-(2, 4-dimethoxybenzylidene) anabaseine (GTS-21) without VNS. The right vagus nerve was exteriorized in all animals. Ventricular fibrillation (VF) was induced and untreated for 8 minutes. Defibrillation was attempted after 8 minutes of CPR. VNS was initiated at the beginning of precordial chest compressions and continued for 4 hours after return of spontaneous circulation (ROSC) in both the VNS and MLA groups. Hemodynamic measurements and myocardial function, including ejection fraction and myocardial performance index, were assessed at baseline, 1 and 4 hours after ROSC. The neurological deficit score was measured at 24-hour intervals for a total of 72 hours. The heart rate was reduced in the VNS and MLA groups, while no difference was found in mean arterial pressure between the four groups. Better post-resuscitation myocardial and cerebral function and longer duration of survival were observed in the VNS-treated animals. The protective effects of VNS could be abolished by MLA and imitated by GTS-21. In addition, VNS decreased the number of electrical shocks and the duration of CPR required. VNS improves multiple outcomes after CPR.

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#28766689   2017/08/02 Save this To Up

Nicotine induces TIPE2 upregulation and Stat3 phosphorylation contributes to cholinergic anti-inflammatory effect.

Cholinergic anti-inflammatory pathway has therapeutic effect on inflammation-associated diseases. However, the exact mechanism of nicotine-mediated anti-inflammatory effect is still unclear. TIPE2, a new member of tumor necrosis factor-α-induced protein-8 family, is a negative regulator of immune homeostasis. However, the roles of TIPE2 in cholinergic anti-inflammatory effect are still uncertain. Here, we demonstrated that nicotine exerts its anti-inflammatory effect by TIPE2 upregulation and phosphorylated stat3 mediated the inhibition of NF-κB activation, which was supported by the following evidence: firstly, both nicotine and TIPE2 inhibit pro-inflammatory cytokine release via NF-κB inactivation. Secondly, nicotine upregulates TIPE2 expression via α7 nicotinic acetylcholine receptor. Moreover, the enhancement of stat3 phosphorylation and decrease of LPS-induced p65 translocation were achieved by nicotine treatment. Importantly, nicotine treatment augments the interaction of phosphorylated stat3 and p65, indicating that the inhibitory effect of nicotine on NF-κB activation was mediated with protein-protein interactions. Hence, this study revealed that TIPE2 upregulation and stat3 phosphorylation contribute to nicotine-mediated anti-inflammation effect, indicating that TIPE2 and stat3 might be potential molecules for dealing with inflammation-associated diseases.

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