Sodium butyrate restores ASC expression and induces apoptosis in LS174T cells

Zhang, Shuai; Bai, Jianzhong; Ren, Shuo; Wang, Ran; Zhang, Li; Zuo, Yongchun

doi:10.3892/ijmm.2012.1156

Cited by 12 publications

(10 citation statements)

References 37 publications

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“…This dose-dependency effect is congruent with the outcome observed in previous experiments and with other inhibitors and pharmacological treatments [19,20]. The results also demonstrate that low, but not higher, doses of NaBu (10 mg/0.5 ml) had an effect on aversive memory extinction, indicating that the NaBu effect is dose-dependent and the inhibitory activity could be mediated by low concentrations that particularly affect histone deacetylation.…”

Section: Discussionsupporting

confidence: 90%

Sodium butyrate into the insular cortex during conditioned taste-aversion acquisition delays aversive taste memory extinction

Núñez-Jaramillo

Reyes-López²,

Miranda³

2014

NeuroReport

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Histone acetylation is one mechanism that promotes gene expression, and it increases during learning of various tasks. Specifically, novel taste consumption produces an increased acetylation of histone lysine residues in the insular cortex (IC), where protein synthesis is crucial during memory consolidation of conditioned taste aversion (CTA). However, the role of this elevated histone acetylation during CTA learning has not been examined directly. Thus, the present study investigated the effects of sodium butyrate (NaBu), a histone deacetylase inhibitor, injected into the IC during CTA acquisition. Male Wistar rats, IC bilaterally implanted, were injected 60 min before saccharine presentation, with a total volume of 0.5 µl of NaBu solution (100, 500, and 10 µg/0.5 µl) or saline; 30 min later animals were injected intraperitoneally with lithium chloride, a malaise-inducing drug. The next day, CTA retrieval was tested. No effects of NaBu were observed during acquisition or retrieval, but during extinction trials, a significant delay in aversive memory extinction was observed in the group injected with the lowest NaBu dose. This result indicates that NaBu in the IC strengthens CTA and delays aversive memory extinction, and suggests that histone acetylation could increase long-term taste-aversive memory strength.

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Section: Discussionsupporting

confidence: 90%

Sodium butyrate into the insular cortex during conditioned taste-aversion acquisition delays aversive taste memory extinction

Núñez-Jaramillo

Reyes-López²,

Miranda³

2014

NeuroReport

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“…Butyrate induces a minimal apoptotic and necrotic effect on MG-63 cells as analyzed by propidium iodide (PI) and annexin V flow cytometry. Other studies have reported the induction of apoptosis on colon cancer cells, B cells and other kinds of cells by butyrate [1,24,25], showing the effect of butyrate may vary by cell type. Ho & Chang (2007) further discovered the toxicity of butyrate on dental pulp cells and its relation to glutathione (GSH) depletion [26].…”

Section: Discussionmentioning

confidence: 99%

“…While mesenchymal stem cells are known to become flattened, spread and to differentiate into osteoblasts [50], butyrate is shown to affect the differentiation of colon cancer cells and osteoblastic cells [1,24,49,51]. Butyrate (0.1 mM) stimulates the expression of mineralization markers in periodontal ligament cells, whereas butyrate exhibits cytotoxicity at concentrations higher than 1 mM [52].…”

Section: Discussionmentioning

confidence: 99%

Butyrate Stimulates Histone H3 Acetylation, 8-Isoprostane Production, RANKL Expression, and Regulated Osteoprotegerin Expression/Secretion in MG-63 Osteoblastic Cells

Chang

Chen

Lian

et al. 2018

IJMS

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Butyric acid as a histone deacetylase (HDAC) inhibitor is produced by a number of periodontal and root canal microorganisms (such as Porphyromonas, Fusobacterium, etc.). Butyric acid may affect the biological activities of periodontal/periapical cells such as osteoblasts, periodontal ligament cells, etc., and thus affect periodontal/periapical tissue destruction and healing. The purposes of this study were to study the toxic effects of butyrate on the matrix and mineralization marker expression in MG-63 osteoblasts. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Cellular apoptosis and necrosis were analyzed by propidium iodide/annexin V flow cytometry. The protein and mRNA expression of osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-B ligand (RANKL) were analyzed by Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR). OPG, soluble RANKL (sRANKL), 8-isoprostane, pro-collagen I, matrix metalloproteinase-2 (MMP-2), osteonectin (SPARC), osteocalcin and osteopontin (OPN) secretion into culture medium were measured by enzyme-linked immunosorbant assay. Alkaline phosphatase (ALP) activity was checked by ALP staining. Histone H3 acetylation levels were evaluated by immunofluorescent staining (IF) and Western blot. We found that butyrate activated the histone H3 acetylation of MG-63 cells. Exposure of MG-63 cells to butyrate partly decreased cell viability with no marked increase in apoptosis and necrosis. Twenty-four hours of exposure to butyrate stimulated RANKL protein expression, whereas it inhibited OPG protein expression. Butyrate also inhibited the secretion of OPG in MG-63 cells, whereas the sRANKL level was below the detection limit. However, 3 days of exposure to butyrate (1 to 8 mM) or other HDAC inhibitors such as phenylbutyrate, valproic acid and trichostatin stimulated OPG secretion. Butyrate stimulated 8-isoprostane, MMP-2 and OPN secretion, but not procollagen I, or osteocalcin in MG-63 cells. Exposure to butyrate (2–4 mM) for 3 days markedly stimulated osteonectin secretion and ALP activity. In conclusion, higher concentrations of butyric acid generated by periodontal and root canal microorganisms may potentially induce bone destruction and impair bone repair by the alteration of OPG/RANKL expression/secretion, 8-isoprostane, MMP-2 and OPN secretion, and affect cell viability. However, lower concentrations of butyrate (1–4 mM) may stimulate ALP, osteonectin and OPG. These effects are possibly related to increased histone acetylation. These events are important in the pathogenesis and repair of periodontal and periapical destruction.

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“…Preclinical studies demonstrated butyrate had anti-CRC activity associated with prevention of DNA methylation. For example, in LS174T colon cancer cells, butyrate decreased cell proliferation and rescued apoptosis-associated speck-like protein (ASC), a proapoptotic protein silenced by DNA methylation in CRC ( 151 ). In HT-29 colon cancer cells, butyrate was found to protect against genotoxicity induced by the secondary bile DCA ( 152 ), and lower DNMT1 levels ( 153 ).…”

Section: Discussionmentioning

confidence: 99%

Mediterranean Diet: Prevention of Colorectal Cancer

et al. 2017

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Colorectal cancer (CRC) is the third most common cancer diagnosis and the second and third leading cause of cancer mortality in men and women, respectively. However, the majority of CRC cases are the result of sporadic tumorigenesis via the adenoma–carcinoma sequence. This process can take up to 20 years, suggesting an important window of opportunity exists for prevention such as switching toward healthier dietary patterns. The Mediterranean diet (MD) is a dietary pattern associated with various health benefits including protection against cardiovascular disease, diabetes, obesity, and various cancers. In this article, we review publications available in the PubMed database within the last 10 years that report on the impact of a MD eating pattern on prevention of CRC. To assist the reader with interpretation of the results and discussion, we first introduce indexes and scoring systems commonly used to experimentally determine adherence to a MD, followed by a brief introduction of the influence of the MD pattern on inflammatory bowel disease, which predisposes to CRC. Finally, we discuss key biological mechanisms through which specific bioactive food components commonly present in the MD are proposed to prevent or delay the development of CRC. We close with a discussion of future research frontiers in CRC prevention with particular reference to the role of epigenetic mechanisms and microbiome related to the MD eating pattern.

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Sodium butyrate restores ASC expression and induces apoptosis in LS174T cells

Cited by 12 publications

References 37 publications

Sodium butyrate into the insular cortex during conditioned taste-aversion acquisition delays aversive taste memory extinction

Sodium butyrate into the insular cortex during conditioned taste-aversion acquisition delays aversive taste memory extinction

Butyrate Stimulates Histone H3 Acetylation, 8-Isoprostane Production, RANKL Expression, and Regulated Osteoprotegerin Expression/Secretion in MG-63 Osteoblastic Cells

Mediterranean Diet: Prevention of Colorectal Cancer

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