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ABSTRACT: Passive smoking is the involuntary inhalation of cigarette smoke (CS) and has an adverse impact on oral health. We examined the effect of CS exposure on caries risk and experimental dental caries.
Experimental dental caries was induced in rat maxillary molars which were inoculated orally with Streptococcus mutans MT8148 and maintained on a cariogenic diet (diet 2000) and high sucrose water during the experimental period. CS-exposed rats were intermittently housed in an animal chamber with whole-body exposure to CS until killed. Whole saliva was collected before CS exposure (day 0) and for 30 days after the start of CS exposure. Saliva secretion was stimulated by administration of isoproterenol and pilocarpine after anesthesia. Maxillary molars were harvested on day 31.
The increase in body weight of the CS-exposed rats was less than that of the control rats. Salivary flow rate, concentration of S. mutans in the stimulated saliva and caries activity score did not significantly differ between 0 and 30 days after the start of CS exposure. Histological examination of the caries-affected area on maxillary molars 30 days after CS exposure showed expansion compared to control rats. In the electron probe microanalysis, no differences were observed between the mineral components of the CS-exposed teeth and the control teeth.
These results suggest that CS exposure expands the caries-affected area in the maxillary molars of the rat.
Caries Research 11/2011; 45(6):561-7. · 2.33 Impact Factor
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ABSTRACT: Macrolide antibiotics are reported to modulate the production of cytokines in various type of cells. We examined the effect of macrolide antibiotics on inflammatory cytokines (IL-6 and IL-8) and chemical mediator (PGE(2)) and also matrix metalloproteinases (MMPs) productions by human gingival fibroblasts (HGFs) treated with lipopolysaccharide (LPS).
The effect of macrolide antibiotics [erythromycin (EM), azithromycin (AZM) and josamycin (JOM)] on HGFs proliferation were examined by MTT assay. HGFs were treated with LPS from Porphyromonas gingivalis (PgLPS) and macrolide antibiotics, and IL-6, IL-8 and PGE(2) levels were evaluated by ELISA. MMPs were detected by gelatin zymography.
AZM slightly but significantly decreased HGFs proliferation, while EM and JOM did not affected. AZM increased PgLPS-induced IL-8 production dose-dependently, while AZM did not alter IL-6 and PGE2 productions. EM and JOM did not altered PgLPS-induced IL-6, IL-8 and PGE(2) productions. All macrolide antibiotics did not alter MMPs production. These results indicate that macrolide antibiotics have no direct anti-inflammatory effect. However, the use of the inhibitors of cell signaling pathway failed to reveal the mechanism that AZM enhanced PgLPS-induced IL-8 production.
These results suggest macrolide antibiotics have an indirect anti-inflammatory effect as a result of their antimicrobial properties. Because AZM increased LPS-induced IL-8 production by HGFs, the possibility is considered that neutrophils may be migrated to periodontal tissue and phagocytize the periodontopathic bacteria more efficiently.
European journal of medical research 08/2009; 14(7):309-14. · 1.13 Impact Factor
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ABSTRACT: Passive smoking is the involuntary inhalation of cigarette smoke (CS) and has an adverse impact on oral health. We examined the effect of CS exposure on saliva and salivary glands (SGs).
Cigarette smoke-exposed rats were intermittently housed in an animal chamber with whole-body exposure to CS until killed. Whole saliva was collected before CS exposure (0 day), and 15 and 30 days after the start of CS exposure. Saliva secretion was stimulated by administration of isoproterenol and pilocarpine after anesthesia. SGs were collected on 31 days.
The increase in body weight of the CS-exposed rats was less than that of the control rats. Salivary flow rates did not differ at 0, 15 or 30 days after the start of CS exposure. However, the amylase and peroxidase activities and total protein content in the saliva were significantly lower in 15-day CS-exposed rats than in 15-day control rats. Histological examination of the SGs of CS-exposed rats showed vacuolar degeneration, vasodilation and hyperemia.
These results suggest that CS exposure has adverse impacts on salivary composition and SGs, which could aggravate the oral environment.
Oral Diseases 07/2009; 15(7):466-71. · 2.49 Impact Factor
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ABSTRACT: Isradipine raises the cytosolic Ca2+ concentration ([Ca2+]i) in human gingival fibroblasts by enhancing Ca2+ influx through the plasma membrane. To research the pathways through which Ca2+ enters the cells, we examined the interactive effects of isradipine and blockers or enhancers of nonselective cation channels (NSCCs) and Na+/Ca2+ exchangers (NCXs). Normal human gingival fibroblast Gin-1 cells were used. The [Ca2+]i was measured with the Ca2+-sensitive fluorescent dye fura-2/AM. Changes in the fluorescence intensity of fura-2 in the cells were recorded with a video-imaging analysis system. Ca2+ antagonists (nifedipine, verapamil, and diltiazem in the concentration range of 1 to 20 microM) other than isradipine also raised the [Ca2+]i. All of the NSCC inhibitors (SK&F 96365, GdCl3, HgCl2 and flufenamic acid), but none of the NCX inhibitors (KB-R 7943 and benzamil), significantly decreased the [Ca2+]i raised by isradipine (3 microM). Neither the Na+ ionophore monensin nor Na+/K+ ATPase inhibitor ouabain had any significant effect on the isradipine-induced [Ca2+]i rise. Taken together, our data indicate that Ca2+ entry through the NSCCs is involved in the isradipine-induced [Ca2+]i rise. The results obtained here play an important role in the development of drugs for etiologic therapy of gingival overgrowth.
European journal of medical research 03/2006; 11(3):93-6. · 1.13 Impact Factor
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ABSTRACT: As it was reported earlier that isradipine, a Ca superset 2+ antagonist of dihydropyridine derivative class, caused regression of nifedipine-induced hyperplasia of human gingiva, experiments were performed to examine whether or not isradipine would solely inhibit the proliferation of cultured gingival fibroblasts. Normal human gingival fibroblast Gin-1 cells were used to test the impact of this medication. Fibroblast proliferation in the presence of isradipine (10 microM) was examined by using the reagent water-soluble tetrazolium-1 (WST-1). The level of basic fibroblast growth factor (bFGF) in the cell-free supernatant of each well was determined by using an enzyme-linked immunosorvent assay (ELISA) kit. The production of type I collagen was assayed by ELISA. Isradipine significantly enhanced the cell proliferation from the second day of the culture period. Also, isradipine raised the level of bFGF in the culture medium. The same concentration, also significantly enhanced the production of type I collagen. In conclusion, we were able to prove that isradipine causes the proliferation of cultured gingival fibroblasts as well as other dihydropyridine-derivative Ca superset 2+ antagonists do. In order to prevent the gingival overgrowth, it is advisable to be very careful in the use of isradipine as a therapy for hypertension and other indications.
European journal of medical research 07/2004; 9(6):313-5. · 1.13 Impact Factor
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ABSTRACT: The present study was undertaken to confirm that L-type Ca(2+) channels are involved in Ca(2+) entry into osteoblastic MC3T3-E1 cells and to examine the effect of SnCl2, a Ca(2+)]-channel activator, on the intracellular Ca(2+)concentration ([Ca(2+)]i). High K(+)concentration-dependently raised the [Ca(2+)]i. All of the L-type Ca(2+)channel blockers used here, such as nifedipine, nicardipine, verapamil, and diltiazem, and CdCl2 (a non-selective blocker) inhibited the high K(+)-induced [Ca(2+)]i rise, but v-conotoxin GVIA (an N-type blocker) and NiCl2(a T-type blocker) had no effect. Application of SnCl2 alone did not change the [Ca(2+)]i. However, in the presence of high K(+), SnCl2 enhanced the high K(+)-induced [Ca(2+)]i rise, which was inhibited by Ca(2+)]-free medium or nifedipine. In the case where high K(+)was applied prior to SnCl2, SnCl2 alone raised the [Ca(2+)]i by itself. In conclusion, MC3T3-E1 cells possess the voltage-dependent L-type Ca(2+)] channels and SnCl2 facilitates the Ca(2+) entry through the L-type ones under the condition of the membrane depolarization. There is the possibility that Ca(2+) release from intracellular Ca(2+) stores is involved in the action of SnCl2.
Cell Calcium 08/2001; 30(1):67-72. · 3.77 Impact Factor
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ABSTRACT: Propylene glycol (PG) is widely used as a solvent for injections. However, there are a few reports describing severe toxic effects of PG on human nervous tissues. To elucidate its mechanism, the present study has been conducted to determine whether PG enhances the release of catecholamine in PC12 cells. When the incubation time was longer than 3 min, PG significantly facilitated the dopamine release. PG (0.2-20 %v/v) concentration-dependently increased the dopamine release and the effects of PG at the concentrations above 1% were significant. High K+ (50 mM) and carbamylcholine (50 microM) increased the dopamine release. High K+ and electrical stimulation augmented the action of PG. Tetrodotoxin (1 microM) had no effect on the PG action. In conclusion, PG enhances the dopamine release. It is suggested that the facilitation of the transmitter release from the motor nerve terminals may be related to the PG-evoked skin twitch.
Research communications in molecular pathology and pharmacology 02/2000; 107(3-4):323-9.
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ABSTRACT: In order to elucidate the mode of excitatory actions of propylene glycol (PG) on nervous tissues, intracellular calcium concentration ([Ca2+]i) of PC12 cells was measured on the video-imaging analysis system with fura-2. PG concentration-dependently (0.1-20%v/v) raised the [Ca2+]i. Hexamethonium and d-tubocurarine inhibited the carbamylcholine-induced [Ca2+]i rise, but these blockers had no effect on PG. High K+ potentiated the action of PG. The extent of the rise induced by PG in the differentiated cells was larger than that in the undifferentiated ones. The findings suggest that the rise in [Ca2+]i is involved in the excitatory effects of PG.
International Journal of Neuroscience 09/1999; 99(1-4):151-7. · 0.97 Impact Factor
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ABSTRACT: Propylene glycol (PG) raises an intracellular calcium concentration ([Ca2+]i) in PC12 cells. The present study has been undertaken to examine whether or not the voltage-dependent Ca2+ channels are involved in the PG-induced rise in [Ca2+]i and, if so, to determine which types participate in it. CdCl2 (50 micro M) and the Ca2+ -free saline depressed the action of PG (0.5 - 10 %v/v)-induced [Ca2+]i rise. Although NiCl2 (50 micro M) at the same concentration as CdCl2, and omega-agatoxin (50 and 300 nM) had no effect on the PG-induced [Ca2+]i rise, each of omega-conotoxin (1 micro M), nifedipine (10 micro M), nicardipine (10 micro M), varapamil (10 micro M) and diltiazem (10 micro M) significantly decreased it. Electrical stimulation and Bay K 8644 (1 micro M) enhanced the PG-induced [Ca2+]i rise. The second phase of the [Ca2]i rise was fallen fast by nicardipine (10 micro M), but not by omega-conotoxin (1 micro M). The results obtained suggested that the Ca2+ influx through the L- and N-type Ca2+ channels are involved in the PG-induced [Ca2+]i rise.
Research communications in molecular pathology and pharmacology 02/1999; 105(3):179-84.
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ABSTRACT: Propylene glycol (PG) has an excitatory effect on the skeletal muscle of the frog. To determine whether PG has a facilitating effect on the neuromuscular transmission of the mammalian as well as on that of the amphibian and to elucidate the mode of action, we have investigated the effects of PG on the neuromuscular junction of the mouse. PG (1.0% v/v) significantly increased the amplitude of endplate potential. PG raised the frequency of miniature endplate potential and increased its amplitude. PG increased the mean quantal content of the endplate potential. These results indicate that PG facilitates the mouse neuromuscular transmission by accelerating the transmitter release from the nerve terminals and by raising the acetylcholine sensitivity of the endplates.
Research communications in molecular pathology and pharmacology 06/1995; 88(2):237-40.
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ABSTRACT: Stannous chloride (SnCl2) facilitates the calcium (Ca) entry into the frog motor nerve terminals. To compare the mode of action of SnCl2 on the Ca channels in the mouse with that in the frog, we investigated the effects of SnCl2 on the inward Ca current at the nerve terminals. SnCl2 (0.1 mM) did not change the second positive component of the action potential (an outward potassium (K) current) at the terminal part of the nerve terminal. SnCl2 (0.1 mM) increased the amplitude of the prolonged negative or positive deflection (an inward Ca current) evoked by treatment with 1 mM tetraethylammonium and 0.1 mM 3,4-diaminopyridine at the terminal or preterminal part of the nerve terminal, respectively. This augmenting effect of SnCl2 was inhibited by cumulative addition of Ca channel blockers, i.e., 0.1 mM CdCl2, 5 mM NiCl2, 5 mM CoCl2, 5 mM MnCl2, or 10 mM MgCl2. From the results obtained, it has been confirmed that SnCl2 facilitates the transmitter release by enhancing the Ca influx at the nerve terminals but not by blocking the K channels and that the mode of action of SnCl2 in the mouse is identical with that in the frog.
Research communications in chemical pathology and pharmacology 06/1994; 84(2):253-6.
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ABSTRACT: Although a mixture composed of 30 microM stannous chloride (SnCl2) and 75 microM tartaric acid (TA) facilitates neuromuscular transmission in the frog, the mixture had no effect on the endplate potential (e.p.p.) in the rat. The present study has been undertaken to determine whether the responses of the mouse (mammalian) to SnCl2 are different from those of the frog (amphibian). The mixture had no effect on the resting potential or the membrane resistance of the muscle fiber. The mixture did not change the e.p.p. amplitude, but TA (75 microM) significantly decreased it. The mixture increased the quantal content of the e.p.p., but TA decreased it. The mixture raised the frequency of the miniature endplate potential (m.e.p.p.) in the high potassium-medium. In normal saline, both the mixture and TA decreased both the m.e.p.p. frequency and its amplitude. These results suggest that SnCl2 itself facilitates the transmitter release from nerve terminals in the mammalian as well as in the amphibian species.
Research communications in chemical pathology and pharmacology 11/1993; 82(1):121-4.
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ABSTRACT: The effects of propylene glycol (PG) on frog nerve-muscle preparations were examined to determine whether it has an effect on neuromuscular transmission and, if so, to elucidate the mode of the action. PG (5%, v/v) increased the twitch tension to over twice the control value. PG at concentrations above 0.2% significantly increased the amplitude of the endplate potential. PG (1%) raised the frequency of the miniature endplate potentials and increased their amplitude. These results show that PG both facilitates transmitter release from the nerve terminals and raises the acetylcholine sensitivity of the muscle endplate.
Food and Chemical Toxicology 10/1993; 31(9):647-50. · 3.00 Impact Factor
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ABSTRACT: We have investigated the interactions between stannous chloride (SnCl2) and calcium (Ca) channel blockers on endplate potentials (e.p.p.) and on miniature endplate potentials (m.e.p.p.) to determine which type of channel (among L-, N-, and T-type) participates in the SnCl2-induced increase in Ca entry into motor nerve terminals. The e.p.p. amplitude augmented by 30 microM SnCl2 was decreased by cumulative addition of 10 microM CdCl2 or 0.5 microM omega-conotoxin but not by 10 microM NiCl2 or 5 microM nicardipine. The SnCl2 (30 microM)-induced rise in m.e.p.p. frequency in high-potassium medium was reduced by 0.5 microM omega-conotoxin but not by 5 microM nicardipine. These results suggest that activation of the N-type Ca channel is involved in the SnCl2-induced increase in Ca entry into the nerve terminals.
Research communications in chemical pathology and pharmacology 03/1992; 75(2):243-6.
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ABSTRACT: Stannous chloride (SnCl2) increases the calcium (Ca) entry into motor nerve terminals through the voltage-dependent Ca channels. The present study has been conducted to determine which type of channel (i.e., L-, N-, or T-type) participates in the Ca entry increased by SnCl2 (0.1 mM)-induced enhancement of the inward Ca current was more strongly inhibited by CdCl2 (50 microM) or omega-conotoxin (0.1 microM) than by NiCl2 (50 microM) or nifedipine (10 microM), respectively. From the results obtained, it is concluded that SnCl2 increases the Ca entry into the nerve terminal by activating the N-type Ca channels.
Research communications in chemical pathology and pharmacology 11/1991; 74(1):125-8.
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ABSTRACT: Effects of stannous chloride (SnCl2, 30-100 microM) on presynaptic currents recorded from frog neuromuscular junctions were investigated to confirm that increased calcium entry is involved in SnCl2-induced facilitation of the evoked transmitter release. After the potassium channel was blocked by tetraethylammonium (0.1 mM) and 3,4-diaminopyridine (10 microM), SnCl2 (0.1 mM) augmented the prolonged positive deflection of the presynaptic action potential ascribable to calcium inward current, which was thereafter suppressed by the addition of cadmium (0.1 mM). These results suggest that SnCl2 enhances the calcium inward current at the motor nerve terminals.
Research communications in chemical pathology and pharmacology 10/1990; 69(3):369-72.
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ABSTRACT: To determine whether Ca2+ participates in the augmentative action of SnCl2 on the transmitter release, we have investigated interactions between SnCl2 and Cd2+, verapamil, or low Ca2+ on endplate potentials (e.p.p.) and have compared the effect of SnCl2 with that of Mg2+ on miniature endplate potentials (m.e.p.p.). SnCl2 increased the e.p.p. amplitude dose-dependently. Cd2+, verapamil and low Ca2+ shifted the dose-response relationship between SnCl2 and the e.p.p. downwards. In contrast to Mg2+, SnCl2 increased the m.e.p.p. frequency with raised K+ concentration in the medium. These results suggest that Ca2+ participates in the SnCl2-induced facilitation of the transmitter release and that SnCl2 enhances the Ca2+ entry into the nerve terminals.
Research communications in chemical pathology and pharmacology 06/1990; 68(2):267-70.
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ABSTRACT: The effects of SnCl2 on potentials recorded extracellularly from motor nerve terminals of the bullfrog were studied to elucidate the mechanism of the SnCl2-induced facilitation of evoked transmitter release. Under conditions in which the muscle preparations were pretreated with d-tubocurarine and tetraethylammonium in a K+-free medium, SnCl2 (50 microM) augmented the prolonged positive deflection ascribed to the inward Ca2+ current, an effect which was reduced by addition of Cd2+. The results suggest that SnCl2 could increase Ca2+ entry into the nerve terminals.
European Journal of Pharmacology 09/1989; 166(3):527-30. · 2.52 Impact Factor
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Shika Kiso Igakkai zasshi = Japanese journal of oral biology 07/1989; 31(3):333-5.
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ABSTRACT: Present study was conducted to elucidate the mechanism of twitch augmentation by stannous ion. Stannous ion increased the amplitude of the endplate potential and moreover, generated repetitive firing of the muscle fiber. These findings suggest that the twitch augmentation by stannous ion may be due not only to recruitment of the muscle fibers but also to a brief tetanic contraction of the individual fibers.
Research communications in chemical pathology and pharmacology 06/1989; 64(2):343-6.
