Muscimol microinjection into cerebellar fastigial nucleus exacerbates stress-induced gastric mucosal damage in rats

Zhu, Jinzhou; Fei, Sujuan; Zhang, Jian‐Fu; Zhu, Sheng-Ping; Liu, Zhang-Bo; Li, Tingting; Xiao, Qiao

doi:10.1038/aps.2012.152

Cited by 9 publications

(3 citation statements)

References 32 publications

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“…In these etherification reactions, hydroxyl groups in the cellulose chains underwent nucleophilic substitution reactions with the epoxy groups at both ends of PEG, forming the alkoxy groups. In our previous study, we prepared the silk fibroin (SF)/SA composite fiber with a double network using PEGDE as crosslinking agent for SF and CaCl 2 for SA, and found that breaking strength of SF/SA composite fiber was improved by 63.6%. We also demonstrated that addition an appropriate amount of PEGDE could reduce the apparent viscosity of the spinning solution and enhance the spinnability of SF/SA composite fibers.…”

Section: Introductionmentioning

confidence: 99%

Improvement in mechanical and hygroscopic properties of modified SA fiber crosslinking with PEGDE

Meng

Zhu

et al. 2018

J of Applied Polymer Sci

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Modified sodium alginate (mSA) fiber is prepared through the wet spinning process using poly(ethylene glycol) diglycidyl ether (PEGDE, the molecular weight of PEGDE is 400) as the crosslinking agent to improve the mechanical and hygroscopic properties. Flowing property of the spinning solution and properties of the mSA fiber are characterized by DV-C digital viscometer, single fiber electronic tensile strength tester and other instruments. Results show that viscosity of the spinning solution dropped firstly, then increased and decreased lastly with increasing PEGDE content in mSA fiber. The optimal value of the tensile strength of mSA fiber is 2.47 cN/dtex increasing by 64.67% compared to pure SA fiber. Both the crosslinking degree and crystallinity of mSA fiber rise first and then descended with the increase of PEGDE content. The hydroscopicity of mSA fiber increase from 30.5% to 70.9% at 20 wt % PEGDE in mSA fiber.

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Section: Introductionmentioning

confidence: 99%

Improvement in mechanical and hygroscopic properties of modified SA fiber crosslinking with PEGDE

Meng

Zhu

et al. 2018

J of Applied Polymer Sci

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“…We chose anti-PCNA antibodies (diluted to 1:100 with PBS) and the polyHRP anti-rabbit IgG as the primary and the secondary antibod-www.nature.com/aps Li TT et al Acta Pharmacologica Sinica npg ies, respectively [31] . The quantitative analysis was performed blinded under a research microscope (Model IX71, Olympus, Tokyo, Japan).…”

Section: Immunohistochemistry Analysismentioning

confidence: 99%

Glutamate microinjection into the hypothalamic paraventricular nucleus attenuates ulcerative colitis in rats

Zhang

Fei

et al. 2013

Acta Pharmacol Sin

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Aim: To investigate the effects of glutamate microinjection into hypothalamic paraventricular nucleus (PVN) on ulcerative colitis (UC) in rats and to explore the relevant mechanisms. Methods: 2,4,6-Trinitrobenzenesulfonic acid (100 mg/kg in 50% ethanol) was instilled into the colon of adult male SD rats to induce UC. A colonic damage score (CDS) was used to indicate the severity of the colonic mucosal damage. The pathological changes in the colonic mucosa were evaluated using immunohistochemistry, Western blotting, biochemical analyses or ELISA. Ten minutes before UC induction, drugs were microinjected into the relevant nuclei in rat brain to produce chemical stimulation or chemical lesion.Results: Microinjection of glutamate (3, 6 and 12 µg) into the PVN dose-dependently decreased the CDS in UC rats. This protective effect was eliminated after kainic acid (0.3 µg) was microinjected into PVN or into the nucleus tractus solitarius (NTS) that caused chemical lesion of these nuclei. This protective effect was also prevented when the AVP-V 1 receptor antagonist DPVDAV (200 ng) was microinjected into the NTS. The discharge frequency of the vagus was markedly decreased following microinjection of glutamate into the PVN. Microinjection of glutamate into the PVN in UC rats significantly increased the cell proliferation and anti-oxidant levels, and decreased the apoptosis and Bax and caspase 3 expression levels and reduced the pro-inflammatory factors in the colonic mucosa. Conclusion: The activation of hypothalamic PVN exerts protective effects against UC, which is mediated by the NTS and vagus. The effects may be achieved via anti-oxidative, anti-apoptotic, and anti-inflammatory factors.

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“…Similarly oral administration of the GABA(A)R agonist abamectin has been demonstrated to be protective against ethanol-induced gastric injury in therat [ 58 ]. However, the injection of the GABA(B)R agonist baclofen or of the GABA(A)R agonist muscimol into cerebellar fastigial nucleus has recently been shown to exacerbate stress-induced gastric mucosal damage in the rat [ 59 , 60 ]. Finally microinjection of L-glutamate into cerebellar interpositus nucleus has recently been shown to prevent gastric ischemia-reperfusion-induced injury in rats and this effect was associated with a significant increase in gastric mucosal blood flow, together with a decrease in gastric cell apoptosis and increase in gastric cell proliferation [ 61 ].…”

Section: Introductionmentioning

confidence: 99%

Gut-Brain Axis in Gastric Mucosal Damage and Protection

Sgambato¹,

Capuano²,

Sullo³

et al. 2016

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BackgroundThe gut-brain axis plays a potential role in numerous physiological and pathological conditions. Several substances link stomach with central nervous system. In particular, hypothalamo-pituitary-adrenocortical axis, thyrotropin-releasing factor-containing nerve fibers and capsaicin-sensitive nerves are principal mediators of the harmful and protective central nervous system-mediated effects on gastric mucosa. Also, existing evidence indicates that nitric oxide, prostaglandins and calcitonin gene-related peptide play a role as final effectors of gastric protection.MethodsWe undertook a structured search of bibliographic databases for peer-reviewed research literature with the aim of focusing on the role of gut-brain axis in gastric damage and protection. In particular, we examined manuscripts dealing with the role of steroids, thyrotropin-releasing hormone, prostaglandins, melatonin, hydrogen sulfide and peptides influencing food intake (i.e. leptin, cholecystokinin, peptide YY, central glucagon–like peptide-1, and ghrelin). Also, the role of GABAergic and glutamatergic pathways in gastric mucosal protection have been examined.ResultsWe found and reviewed 61 peer-reviewed papers dealing with the major aspects related to the role of gut brain axis in gastric mucosal damage and protection.ConclusionsA dense neuronal network links stomach with central nervous system and a number of neurotransmitters and peptides functionally and anatomically related to central nervous system play a major role in contributing to gastric mucosal integrity.Exploiting the mechanisms underlying the connection between brain and gut may lead to a better understanding of the pathophysiology of gastric mucosal injury and to an improvement in the prevention and, eventually, management of gastric damage.

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Muscimol microinjection into cerebellar fastigial nucleus exacerbates stress-induced gastric mucosal damage in rats

Cited by 9 publications

References 32 publications

Improvement in mechanical and hygroscopic properties of modified SA fiber crosslinking with PEGDE

Improvement in mechanical and hygroscopic properties of modified SA fiber crosslinking with PEGDE

Glutamate microinjection into the hypothalamic paraventricular nucleus attenuates ulcerative colitis in rats

Gut-Brain Axis in Gastric Mucosal Damage and Protection

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