scholarly journals Diazepam Enhances Production of Diazepam-Binding Inhibitor (DBI), a Negative Saliva Secretion Regulator, Localized in Rat Salivary Gland

2011 ◽  
Vol 115 (2) ◽  
pp. 221-229 ◽  
Author(s):  
Eri Tsukagoshi ◽  
Mitsuru Kawaguchi ◽  
Takashi Shinomiya ◽  
Masanobu Yoshikawa ◽  
Toshihiko Kawano ◽  
...  
Keyword(s):  
Salivary Gland ◽  
Saliva Secretion ◽  
Rat Salivary Gland

scholarly journals Choline Acetyltransferase Induces the Functional Regeneration of the Salivary Gland in Aging SAMP1/Kl -/- Mice

2021 ◽  
Vol 22 (1) ◽  
pp. 404
Author(s):  
Nguyen Khanh Toan ◽  
Nguyen Chi Tai ◽  
Soo-A Kim ◽  
Sang-Gun Ahn
Keyword(s):  
Salivary Gland ◽  
Choline Acetyltransferase ◽  
Salivary Flow ◽  
Salivary Secretion ◽  
Functional Markers ◽  
Tooth Structure ◽  
Saliva Secretion ◽  
Gland Function ◽  
The Impact

Salivary gland dysfunction induces salivary flow reduction and a dry mouth, and commonly involves oral dysfunction, tooth structure deterioration, and infection through reduced salivation. This study aimed to investigate the impact of aging on the salivary gland by a metabolomics approach in an extensive aging mouse model, SAMP1/Klotho -/- mice. We found that the salivary secretion of SAMP1/Klotho -/- mice was dramatically decreased compared with that of SAMP1/Klotho WT (+/+) mice. Metabolomics profiling analysis showed that the level of acetylcholine was significantly decreased in SAMP1/Klotho -/- mice, although the corresponding levels of acetylcholine precursors, acetyl-CoA and choline, increased. Interestingly, the mRNA and protein expression of choline acetyltransferase (ChAT), which is responsible for catalyzing acetylcholine synthesis, was significantly decreased in SAMP1/Klotho -/- mice. The overexpression of ChAT induced the expression of salivary gland functional markers (α–amylase, ZO-1, and Aqua5) in primary cultured salivary gland cells from SAMP1/Klotho +/+ and -/- mice. In an in vivo study, adeno-associated virus (AAV)-ChAT transduction significantly increased saliva secretion compared with the control in SAMP1/Klotho -/- mice. These results suggest that the dysfunction in acetylcholine biosynthesis induced by ChAT reduction may cause impaired salivary gland function

Hyperglycemia Induces Generation of Reactive Oxygen Species and Accelerates Apoptotic Cell Death in Salivary Gland Cells

Pathobiology ◽  
2021 ◽  
pp. 1-8
Author(s):  
Naoyuki Matsumoto ◽  
Daisuke Omagari ◽  
Ryoko Ushikoshi-Nakayama ◽  
Tomoe Yamazaki ◽  
Hiroko Inoue ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Salivary Gland ◽  
Tissue Injury ◽  
Ros Production ◽  
Oxygen Species ◽  
Saliva Secretion ◽  
Salivary Gland Tissue ◽  
Gland Tissue

<b><i>Introduction:</i></b> Type-2 diabetes mellitus (T2DM) is associated with several systemic vascular symptoms and xerostomia. It is considered that hyperglycemia-induced polyuria and dehydration cause decreased body-water volume, leading to decreased saliva secretion and, ultimately, xerostomia. In T2DM, increased production of reactive oxygen species (ROS) causes tissue damage to vascular endothelial cells as well as epithelial tissue, including pancreas and cornea. Hence, a similar phenomenon may occur in other tissues and glands in a hyperglycemic environment. <b><i>Methods:</i></b> Salivary gland tissue injury was examined, using T2DM model mouse (db/db). Transferase‐mediated dUTP nick‐end labeling (TUNEL) was conducted to evaluate tissue injury. The levels of malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine, Bax/Bcl-2 ratio were measured as indicator of oxidative stress. Moreover, in vitro ROS production and cell injury was evaluated by mouse salivary gland-derived normal cells under high-glucose condition culture. <b><i>Results:</i></b> In vivo and in vitro analysis showed a higher percentage of TUNEL-positive cells and higher levels of MDA and 8-hydroxy-2′-deoxyguanosine in salivary gland tissue of db/db mice. This suggests damage of saliva secretion-associated lipids and DNA by hyperglycemic-induced oxidative stress. To analyze the mechanism by which hyperglycemia promotes ROS production, mouse salivary gland-derived cells were isolated. The cell culture with high-glucose medium enhanced ROS production and promotes apoptotic and necrotic cell death. <b><i>Conclusion:</i></b> These findings suggest a novel mechanism whereby hyperglycemic-induced ROS production promotes salivary gland injury, resulting in hyposalivation.

scholarly journals Radiation Produces Irreversible Chronic Dysfunction in the Submandibular Glands of the Rat

2012 ◽  
Vol 6 (1) ◽  
pp. 8-13 ◽  
Author(s):  
C De la Cal ◽  
J Fernández-Solari ◽  
CE Mohn ◽  
JP Prestifilippo ◽  
A Pugnaloni ◽  
...  
Keyword(s):  
Single Dose ◽  
Salivary Gland ◽  
Ionizing Radiation ◽  
Salivary Secretion ◽  
Maximal Response ◽  
Chronic Effect ◽  
Post Irradiation ◽  
Gland Function ◽  
High Doses ◽  
Rat Salivary Gland

The exposure to high doses of ionizing radiation during radiotherapy results in severe morphological and functional alterations of the salivary glands, such as xerostomia. In the present study we investigated the chronic effect of a single radiation dose of 15 Gray (Gy) limited to head and neck on rat salivary gland function (salivary secretion and gland mass) and histology. Results indicate that norepinephrine (NE)-induced salivary secretion was reduced significantly at 30, 90, 180 and 365 days after the administration of a single dose of 15 Gy of ionizing radiation compared to non-irradiated animals. The maximal secretory response was reduced by 33% at 30 and 90 days post irradiation. Interestingly, a new fall in the salivary response to NE was observed at 180 days and was maintained at 365 days post irradiation, showing a 75% reduction in the maximal response. The functional fall of the salivary secretion observed at 180 days post irradiation was not only associated with a reduction of gland mass but also to an alteration of the epithelial architecture exhibiting a changed proportion of ducts and acini, loss of eosinophilic secretor granular material, and glandular vacuolization and fibrosis. On the basis of the presented results, we conclude that ionizing radiation produces irreversible and progressive alterations of submandibular gland (SMG) function and morphology that leads to a severe salivary hypo-function.

Effects of surgical ovariectomy on rat salivary gland function

1993 ◽  
Vol 38 (9) ◽  
pp. 779-784 ◽  
Author(s):  
Karnam R. Purushotham ◽  
Pao-Li Wang ◽  
Calogero Dolce ◽  
Tivadar Zelles ◽  
Josef Blazsek ◽  
...  
Keyword(s):  
Salivary Gland ◽  
Salivary Gland Function ◽  
Gland Function ◽  
Rat Salivary Gland

Rate of protein synthesis in rat salivary gland cells after pilocarpine or feeding

1975 ◽  
Vol 164 (4) ◽  
pp. 447-456 ◽  
Author(s):  
A. H. Kuijper-Lenstra ◽  
M. F. Kramer ◽  
W. J. van Venrooij
Keyword(s):  
Protein Synthesis ◽  
Salivary Gland ◽  
Gland Cells ◽  
Salivary Gland Cells ◽  
Rat Salivary Gland

scholarly journals Inhibition of Alk signaling promotes the induction of human salivary-gland-derived organoids

2020 ◽  
Vol 13 (9) ◽  
pp. dmm045054 ◽  
Author(s):  
Shohei Yoshimoto ◽  
Junko Yoshizumi ◽  
Hiromasa Anzai ◽  
Koichiro Morishita ◽  
Kazuhiko Okamura ◽  
...  
Keyword(s):  
Salivary Gland ◽  
Fungal Infections ◽  
Disease Model ◽  
Good Health ◽  
Functional Changes ◽  
Human Salivary Gland ◽  
Saliva Secretion ◽  
Tnf Α

ABSTRACTHyposalivation and xerostomia are the cause of several morbidities, such as dental caries, painful mucositis, oral fungal infections, sialadenitis and dysphagia. For these reasons, preservation of normal saliva secretion is critical for the maintenance of functionally normal oral homeostasis and for keeping good health. Several strategies for restoring salivary gland function have been reported, from different points of view, based on the use of salivary-gland-derived epithelial stem/progenitor cells and tissue engineering approaches to induce organoids that mimic in vivo salivary glands. In this study, we clarified that inhibition of activin receptor-like kinase (Alk) signaling was essential for the induction of human salivary-gland-derived organoids, and demonstrated the usefulness of such organoids as an inflammatory disease model. In inflammatory conditions like sialadenitis, in general, pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α, also known as TNF) are upregulated, but their function is still unclear. In our established human salivary-gland-derived organoid culture system, we successfully induced organoid swelling by stimulation with carbachol, a non-selective cholinergic agonist, and forskolin, an activator of cystic fibrosis transmembrane conductance regulator (CFTR). Furthermore, we found that this organoid swelling was inhibited by TNF-α. From these results, we could clarify the inhibitory function of TNF-α on saliva secretion in vitro. Thus, our established human salivary-gland-derived organoids would be useful for in vitro analyses of the morphological and functional changes involved in salivary gland dysfunctions in several research fields, such as pathobiology, inflammation and regenerative medicine.This article has an associated First Person interview with the first author of the paper.

Facilitation of noradrenaline release by gallamine in the rat salivary gland

1985 ◽  
Vol 331 (2-3) ◽  
pp. 220-224 ◽  
Author(s):  
Ravindra K. Malhotra ◽  
Taruna D. Wakade ◽  
Arun R. Wakade
Keyword(s):  
Salivary Gland ◽  
Noradrenaline Release ◽  
Rat Salivary Gland
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