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Butyric Acid Induces Apoptosis in Inflamed Fibroblasts

¹ Department of Microbiology and Immunology, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba 271-8587, Japan;
² Department of Microbiology and
³ Department of Biochemistry, Nihon University School of Dentistry, Tokyo 101-8310, Japan; and
⁴ Department of Infectious Diseases, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka 431-3192, Japan

View larger version (45K): [in this window] [in a new window]   Figure 1. Effects of short-chain fatty acids on the viability of gingival fibroblasts. Healthy (Gin-1, N23, N32, and GF7) and inflamed (F22-G, F33-G, M38-G, and F42-G) gingival fibroblasts were cultured with (A) the indicated concentrations of butyric acid, (B) 5 mM volatile fatty acids, or (C) 5 mM non-volatile fatty acids. Cell viability was determined by the MTT assay and expressed as a percentage of the absorbance obtained in the absence of fatty acids. The results are expressed as the mean ± standard error of 3 independent experiments. *P < 0.01 vs. untreated control cells (white bar).

View larger version (54K): [in this window] [in a new window]   Figure 2. Butyric-acid-induced apoptosis in inflamed gingival fibroblasts. Healthy (Gin-1, N23, N32, and GF7) and inflamed (F22-G, F33-G, M38-G, and F42-G) gingival fibroblasts were cultured (A) with the indicated concentrations of butyric acid for 24 hrs and (B) in the presence of 5 mM butyric acid for the indicated time periods. Harvested cells were stained with DAPI. The results are expressed as the mean ± standard error of 3 independent experiments. (C) Agarose gel electrophoresis of DNA. Healthy (Gin-1, N23, and GF7) and inflamed (F22-G, F33-G, M38-G, and F42-G) gingival fibroblasts were cultured in the absence (lanes 1, 3, 5, 7, 9, 11, and 13) or presence (lanes 2, 4, 6, 8, 10, 12, and 14) of 5 mM butyric acid (BA). (D) Nuclear morphology of gingival fibroblasts treated with butyric acid. HGF (N23, upper panels) and IGF (M38-G, lower panels) were cultured in the absence (left panels) or presence (right panels) of 5 mM butyric acid (BA) and stained with DAPI. The results are representative of 3 independent experiments. Scale bars, 10 µm.

View larger version (20K): [in this window] [in a new window]   Figure 3. Mitochondrial membrane potential (MMP) and effects of caspase inhibitors on the butyric-acid-induced apoptosis of inflamed gingival fibroblasts. (A) Healthy (Gin-1 and N23) and inflamed (F22-G and M38-G) gingival fibroblasts were treated with 5 mM butyric acid, and the MMP was measured as the fluorescence emitted by rhodamine 123 taken up by the mitochondria. Data are expressed as a percentage of the control (mean ± standard error [SE]). *P < 0.01 vs. corresponding control cells (Gin 1 and N23). (B) Inflamed gingival fibroblasts (F22-G and M38-G) were pre-treated with caspase inhibitors and then treated with 5 mM butyric acid. Harvested cells were stained with DAPI. *P < 0.01 vs. inhibitor-free butyric-acid-treated control cells. The results are expressed as the mean ± SE of 3 independent experiments.

Journal of Dental Research, Vol. 87, No. 1, 51-55 (2008)
DOI: 10.1177/154405910808700108


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