Pharmacological evidences for the stimulation of calcium-sensing receptors by nifedipine in gingival fibroblasts.

Objective: To investigate pharmacologically whether CaSRs are involved in the Ca(2+) antagonist-induced [Ca(2+)]i elevation in gingival fibroblasts.

Materials And Methods: Gin-1 cells, normal human gingival fibroblasts, were used as the material. The [Ca(2+)] i was measured with fura-2/AM, a Ca(2+)-sensitive fluorescent dye.

Preventive effects of a kampo medicine, orento on inflammatory responses in lipopolysaccharide treated human gingival fibroblasts.

In the present study, we investigated the effects of a Kampo medicine Orento (TJ-120) on the production of prostaglandin E(2) (PGE(2)), interleukin (IL)-6 and IL-8 by human gingival fibroblasts (HGFs) treated with lipopolysaccharide from Porphyromonas gingivalis (PgLPS). HGFs proliferation was dose-dependently decreased with Orento at days 3 and 7. However, treatment with PgLPS (10 ng/ml), Orento (up to 1 mg/ml) and their combinations for 24 h did not affect the viability of HGFs.

Preventive effects of a Kampo medicine, Shosaikoto, on inflammatory responses in LPS-treated human gingival fibroblasts.

In the present study, we investigated the anti-inflammatory effects of a Kampo medicine Shosaikoto (TJ-9) using in vitro periodontal disease model, in which human gingival fibroblasts (HGFs) treated with lipopolysaccharide (LPS) from Porphyromonas gingivalis (PgLPS) produce IL-6, IL-8 and prostaglandin E2 (PGE2). Treatment with PgLPS (10 ng/ml), TJ-9 (up to 1 mg/ml) and their combinations for 24 h did not affect the viability of HGFs. Moreover, TJ-9 did not alter LPS-induced IL-6 and IL-8 productions.

Elevation of cytosolic calcium level triggers calcium antagonist-induced gingival overgrowth.

Calcium (Ca2+) antagonists induce gingival overgrowth as a side effect but the pathogenic mechanism is still unknown. The Ca2+-channel activator Bay K 8644 elevates intracellular Ca2+ concentration ([Ca2+]i) and enhances the cell proliferation of gingival fibroblasts in a dose-dependent manner. Verapamil, an L-type Ca2+-channel blocker, also elevates [Ca2+]i in gingival fibroblasts, but it has no effect on other fibroblasts such as those of the lung, skin, and muscle.

Calcium antagonists cause dry mouth by inhibiting resting saliva secretion.

Ca2+ antagonists cause dry mouth by inhibiting saliva secretion. The present study was undertaken to elucidate the mechanism by which Ca2+ antagonists cause dry mouth. Since the intracellular Ca2+ concentration ([Ca2+]i) is closely related to saliva secretion, [Ca2+]i was measured with a video-imaging analysis system by using human submandibular gland (HSG) cells as the material.

Involvement of Na(+)-K(+)-2Cl(-) cotransporters in hypertonicity-induced rise in intracellular calcium concentration.

A hypertonic saline containing propylene glycol facilitates calcium (Ca(2+)) influx through voltage-dependent Ca(2+) channels. The present study performed experiments to elucidate the mechanism by which Na(+)-K(+)-2Cl(-) cotransporters participate in the rise in the intracellular calcium concentration ([Ca(2+)]i) under the hypertonic condition. Both furosemide and ethacryonic acid significantly decreased the [Ca(2+)]i raised by hypertonicity.

Inhibition of nifedipine-induced proliferation of cultured human gingival fibroblasts by Saiko, a Chinese herbal medicine.

Saiko is predominantly contained in Saireito, a Chinese herbal medicine. The present study was conducted to determine whether or not Saiko is involved in the inhibition by Saireito of nifedipine-induced proliferation and collagen synthesis in gingival fibroblasts. Nifedipine (10 microM) significantly enhanced the proliferation starting on day 5 of the culture period.

Participation of tyrosine kinase and phospholipase Cgamma in isradipine-induced proliferation of cultured human gingival fibroblasts.

Some kinds of drugs such as calcium (Ca(2+)) channel antagonists, antiepileptics and immunosuppressants cause gingival overgrowth as a side effect, the mechanism of which is still unclear. We have examined the effects of isradipine, one of the dihydropyridine-derivative Ca(2+) channel antagonists, on cultured human gingival fibroblast Gin-1 cells. In the present study, to elucidate the mechanism by which isradipine causes gingival overgrowth, we examined whether tyrosine kinase (TK) and phopholipase Cgamma (PLCgamma) are involved in the isradipine-induced proliferation of gingival fibroblasts.

Prostaglandin E2 receptors EP2 and EP4 are down-regulated during differentiation of mouse osteoclasts from their precursors.

Prostaglandin E2 (PGE2) has been proposed to be a potent stimulator of bone resorption. However, PGE2 itself has been shown to directly inhibit bone-resorbing activity of osteoclasts. We examined the role of PGE2 in the function of mouse osteoclasts formed in vitro.

Rise in intracellular calcium concentration elicited by isradipine in Gin-1 cells.

We performed experiments to examine whether isradipine (Isr), a calcium antagonist, would raise the intracellular calcium concentration ([Ca2+]i) in Gin-1 cells and, if so, to elucidate the mechanism of the [Ca2+]i rise. Gin-1 cells, which are human normal gingival fibroblasts were used as the material. The [Ca2+]i was measured with the Ca2+-sensitive fluorescent dye fura-2/AM.

Inhibition by tranilast of nifedipine-induced proliferation of cultured human gingival fibroblasts.

The appropriate method of etiologic therapy for gingival overgrowth is yet unknown. In this study drug-induced proliferation of Gin-1 cells, a normal human gingival fibroblast cell line, was examined by using the reagent water-soluble tetrazolium-1. Tranilast (100 microM) inhibited the nifedipine (10 microM)-induced proliferation of gingival fibroblasts.