Expression of NADPH-d in the vagal nuclei of the chronic esophagitis model in rats

Doshi, Pooja; Srivastava, G.

doi:10.3906/sag-1209-30

Cited by 3 publications

(3 citation statements)

References 57 publications

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“…Previous experiments by our group have shown that c-fos expression significantly increased in the NTS/DMV and AP in rats receiving an acid plus pepsin perfusion [10]. The proposed mechanism was that exposure of the lower part of the esophagus to acid-pepsin stimulated the mucosal receptors, which in turn activated the neurons of the NTS and then of the DMV to modulate esophageal peristalsis [11].…”

Section: Introductionmentioning

confidence: 99%

Destruction of the Dorsal Motor Nucleus of the Vagus Aggravates Inflammation and Injury from Acid-Induced Acute Esophagitis in a Rat Model

Zhao

Xie

Geng

et al. 2019

Analytical Cellular Pathology

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Background/Aims. The aim of this study is to examine the protective effect of the cholinergic anti-inflammatory pathway (CAP) in experimental esophagitis in rats. Methods. A total of 40 male Sprague-Dawley (SD) rats were randomly divided into five groups as follows: control group, sham + saline group, sham + acid group, operation + saline group, and operation + acid group. Two weeks after the dorsal motor nucleus of the vagus (DMV) destruction, hydrochloric acid with pepsin was perfused into the lower part of the esophagus for 90 min. The rats were sacrificed 60 min after perfusion. The esophagus was prepared for hematoxylin and eosin (HE) staining, and the degree of inflammation and NF-κB activation in the esophagus was measured. Inflammatory cytokines (TNF-α, IL-6, IL-1β, and PGE2) in the esophagus were measured by ELISA. The brain was removed and processed for c-fos immunohistochemistry staining. The c-fos-positive neurons were counted and analyzed. Results. The TNF-α, IL-1β, IL-6, and PGE2 concentrations in the esophageal tissue increased after acid perfusion. The microscopic esophagitis scores and the activation of NF-κB p65 in the esophagus were significantly higher in the operation + acid group than in the operation + saline group. c-fos-positive neurons significantly increased in rats receiving acid perfusion in the amygdala (AM), the paraventricular nucleus of the hypothalamus (PVN), the parabrachial nucleus (PBN), the nucleus of the solitary tract (NTS)/DMV, the nucleus ambiguous (NA), the reticular nucleus of the medulla (RNM), and the area postrema (AP). After DMV destruction, c-fos expression was reduced in the AM, PVN, PBN, NTS/DMV, NA, RNM, and AP, especially in the AM, PVN, NTS/DMV, RNM, and AP. Conclusions. The DMV is an important nucleus of the CAP. The DMV lesion can aggravate esophageal inflammation and injury from acid-induced acute esophagitis in a rat model. The CAP has a protective effect on the acute esophagitis rat model and could be a new therapy for reflux esophagitis (RE).

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Section: Introductionmentioning

confidence: 99%

Destruction of the Dorsal Motor Nucleus of the Vagus Aggravates Inflammation and Injury from Acid-Induced Acute Esophagitis in a Rat Model

Zhao

Xie

Geng

et al. 2019

Analytical Cellular Pathology

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“…In rats, nitric oxide synthase (NOS)-containing abdominalprojecting vagal preganglionic cell bodies are present mainly within the caudal and rostral regions of DMV (23,38,56), and microinjection of L-arginine into the DVC decreases intragastric pressure (23) via an excitatory effect on DMV neurons (46). In rodents, apelin is known to activate the L-arginine-NOS pathway in peripheral vasculature (22,57), and more importantly, recent studies have shown that central administration of apelin induces hypothalamic NO release in mice (14,16).…”

Section: Discussionmentioning

confidence: 99%

Apelin-13 inhibits gastric motility through vagal cholinergic pathway in rats

Bülbül

Sinen

Gök

et al. 2018

American Journal of Physiology-Gastrointestinal and Liver Physi

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The expression of apelin and its receptors (APJ) in central autonomic networks suggests that apelin may regulate gastrointestinal motor functions. In rodents, central administration of apelin-13 has been shown to inhibit gastric emptying; however, the mechanisms involved remain to be determined. Using male adult Sprague-Dawley rats, the aims of the present study were 1) to determine the expression of APJ receptor in the dorsal vagal complex (DVC), 2) to assess the effects of central application of apelin-13 into the DVC on gastric tone and motility, and 3) to investigate the neuronal pathways responsible for apelin-induced alterations. APJ receptor immunoreactivity was detected in gastric-projecting and choline acetyltransferase-positive neurons of the DVC. Microinjection of apelin-13 into the DVC significantly decreased gastric tone and motility in both corpus and antrum. The apelin-induced reduction in gastric tone and motility was prevented by surgical vagotomy or fourth ventricular application of the APJ receptor antagonist, [Ala13]apelin-13 (F13A). Systemic administration of the muscarinic receptor antagonist atropine, but not the nitric oxide synthase inhibitor nitro-l-arginine methyl ester (l-NAME), abolished the apelin-induced inhibitory responses. The present results indicate a central modulatory role of apelin in the vagal neurocircuitry that controls gastric motor functions via withdrawal of the tonically active cholinergic pathway. NEW & NOTEWORTHY This is the first study investigating the effects induced by brain stem application of apelin-13 while monitoring gastric tone and motility in rats. We have found that gastric-projecting neurons of the dorsal vagal complex express apelin receptors (APJ), which mediate the inhibitory actions of apelin-13. The inhibitory effects of apelin were abolished by systemic preadministration of atropine, but not nitro-l-arginine methyl ester (l-NAME). Apelin seems to modulate gastric motility via withdrawal of the tonically active vagal cholinergic pathway.

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“…Aktivitas enzim NOS dijadikan dasar metode histokimia sederhana untuk menggambarkan sel yang mengandung NOS yaitu dengan pewarnaan NADPH-d (Sehirli et al, 2014;Benesova et al, 2004). Kerusakan mukosa sekum menyebabkan masuknya kalsium (Ca 2+ ) ke dalam dinding sekum, sebagai akibatnya potensial aksi dalam sel-sel ganglion mienterik meningkat.…”

Section: Hasil Dan Pembahasanunclassified

"Profil Saraf Nitrergik Sekum Ayam Pedaging yang Diinfeksi Eimeria tenella (THE PROFILE OF NEORAL NITRERGIC IN THE COECUM OF BROILER INFECTED WITH Emeria tenella)"

Hana

Astuti²,

Fibrianto³

et al. 2015

jveteriner

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Neurotrasmitter yang terdapat pada sistem saraf enterik berperan penting dalam berbagai enteropati, termasuk radang pada usus. Beberapa laporan telah membuktikan bahwa keradangan dapat mengubah neuron nitrergik. Tujuan dilakukannya penelitian ini adalah untuk mengetahui profil saraf nitrergik pada sekum ayam pedaging yang diinfeksi oleh Eimeria tenella dan pewarnaan Nicotinamide Adenine Dinucleotide Phosphate-diaphorase (NADPH-d). Hewan percobaan yang digunakan dalam penelitian ini adalah 36 ekor ayam umur dua minggu yang sehat dan bebas koksidiosis. Seluruh ayam percobaan diadaptasikan dengan kondisi kandang selama tujuh hari dengan pakan dan air minum diberikan secara ad libitum. Ayam percobaan dibagi secara acak menjadi tiga kelompok masing-masing kelompok berjumlah 12 ekor. Ayam kelompok I tidak diinfeksi dengan oosista hanya diberi 1,0 mL akuades/ekor peroral, kelompok II diinfeksi dosis tunggal 5x10 3 oosista/ekor peroral, dan kelompok III diinfeksi dosis tunggal 2x10 4 oosista/ekor peroral. Pada hari ke-7 pascainfeksi, seluruh ayam dipuasakan selama 12 jam, kemudian dikorbankan nyawanya, dinekropsi dan diambil jaringan sekumnya. Sampel sekum dinilai skor pelukaannya. Sampel jaringan sekum dibuat preparat histokimia dengan menggunakan pewarnaan NADPH-d untuk mengetahui perubahan morfometrik neuron nitrergiknya. Hasil penelitian menunjukkan bahwa skor pelukaan sekum kelompok I= 0, kelompok II=2+, kelompok III= 3+. Kepadatan neuron pada sekum ayam kelompok I=2794,96±4,65 neuron/cm 2 , kelompok II=4930,36±63,73 neuron/cm 2 , dan kelompok III=7892,31±44,97 neuron/cm 2. Kepadatan neuron kelompok II dan III meningkat sangat signifikan (p<0,01) dibanding kelompok I. Kepadatan neuron nitrergik kelompok III meningkat signifikan dibanding kelompok II (P<0,05). Disimpulkan bahwa infeksi E. tenella menyebabkan peningkatan jumlah neuron mienterik nitrergik sekum ayam. Semakin tinggi tingkatan skor pelukaan sekum semakin meningkat jumlah neuron mienterik nitrergik sekum.

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Expression of NADPH-d in the vagal nuclei of the chronic esophagitis model in rats

Cited by 3 publications

References 57 publications

Destruction of the Dorsal Motor Nucleus of the Vagus Aggravates Inflammation and Injury from Acid-Induced Acute Esophagitis in a Rat Model

Destruction of the Dorsal Motor Nucleus of the Vagus Aggravates Inflammation and Injury from Acid-Induced Acute Esophagitis in a Rat Model

Apelin-13 inhibits gastric motility through vagal cholinergic pathway in rats

"Profil Saraf Nitrergik Sekum Ayam Pedaging yang Diinfeksi Eimeria tenella (THE PROFILE OF NEORAL NITRERGIC IN THE COECUM OF BROILER INFECTED WITH Emeria tenella)"

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