Understanding activity of butyrate at a cellular level

Butyrate is a short-chain fatty acid of four carbons in length that is a by-product produced by the microbial fermentation of dietary fiber and undigested carbohydrates within the colon.Over the years,butyrate has attracted significant attention due to its diverse roles within cells.

Effects of coagulation bath temperature on structure and performance of poly(vinyl butyral) hollow fiber membranes via thermally induced phase separation

Poly （vinyl butyral） （PVB） hollow fiber membranes were fabricated via thermally induced phase separation （TIPS）. The effects of coagulation bath temperature （CBT） on the structure and performance of membranes were investigated in detail. The morphologies of the membranes were studied by scanning electron microscopy （SEM）, the performances of water permeability, rejection, breaking strength and elongation were measured, respectively. The results indicate that all the membranes have the asymmetric morphology and the thickness of the skin layer decreases and the pore size of the outer layer increases with the increase of CBT. The permeability of membranes prepared at air gap 1.0 cm and take-up speed 0.253 m/s increases from 1.047×10-7 to 5.909×10-7 m3/（m2·s-kPa） with the CBT increasing from 20 ℃ to 40℃, and sharply increases to 35.226×10 7 m3/（m2.s.kPa）once the CBT arrives at 50 ℃. While the carbonic ink rejections have no significant decrease, totally exceed 98%, but that of acid-maleic acid copolymer greatly decreases with the increase of CBT. Both the breaking strength and elongation decrease with the increase of CBT.

Dietary sodium acetate and sodium butyrate improve high-carbohydrate diet utilization by regulating gut microbiota, liver lipid metabolism, oxidative stress, and inflammation in largemouth bass(Micropterus salmoides)

Background Adequate level of carbohydrates in aquafeeds help to conserve protein and reduce cost. However, studies have indicated that high-carbohydrate(HC) diet disrupt the homeostasis of the gut–liver axis in largemouth bass, resulting in decreased intestinal acetate and butyrate level.Method Herein, we had concepted a set of feeding experiment to assess the effects of dietary sodium acetate(SA) and sodium butyrate(SB) on liver health and the intestinal microbiota in largemouth bass fed an HC diet. The experimental design comprised 5 isonitrogenous and isolipidic diets, including LC(9% starch), HC(18% starch), HCSA(18% starch;2 g/kg SA), HCSB(18% starch;2 g/kg SB), and HCSASB(18% starch;1 g/kg SA + 1 g/kg SB). Juvenile largemouth bass with an initial body weight of 7.00 ± 0.20 g were fed on these diets for 56 d.Results We found that dietary SA and SB reduced hepatic triglyceride accumulation by activating autophagy(ATG101, LC3B and TFEB), promoting lipolysis(CPT1α, HSL and AMPKα), and inhibiting adipogenesis(FAS, ACCA, SCD1 and PPARγ). In addition, SA and SB decreased oxidative stress in the liver(CAT, GPX1α and SOD1) by activating the Keap1-Nrf2 pathway. Meanwhile, SA and SB alleviated HC-induced inflammation by downregulating the expression of pro-inflammatory factors(IL-1β, COX2 and Hepcidin1) through the NF-κB pathway. Importantly, SA and SB increased the abundance of bacteria that produced acetic acid and butyrate(Clostridium_sensu_stricto_1). Combined with the KEGG analysis, the results showed that SA and SB enriched carbohydrate metabolism and amino acid metabolism pathways, thereby improving the utilization of carbohydrates. Pearson correlation analysis indicated that growth performance was closely related to hepatic lipid deposition, autophagy, antioxidant capacity, inflammation, and intestinal microbial composition.Conclusions In conclusion, dietary SA and SB can reduce hepatic lipid deposition;and alleviate oxidative stress and inflammation in largemouth bass fed on HC diet. These beneficial effects may be due to the altered composition of the gut microbiota caused by SA and SB. The improvement effects of SB were stronger than those associated with SA.

Rheological properties of polyvinyl butyral/Pluronic F127/PEG200 blend systems

The influence of temperature and mass fraction of Pluonic F127 on the rheological properties of polyvinyl butyric （PVB）/Pluronic F127/polyethylene glycol （PEG） 200 blend systems was investigated by a rotational rheometer with parallel plates. The results show that the blend systems approach homogeneous state at 140, 150 and 160℃while the rheological properties of the blend systems significantly deviate from the homogeneous systems at 120℃. Shear thinning behavior is observed for all the blend systems at different temperatures and is enhanced by increasing Pluronic F127 content. The complex viscosity, storage modulus, loss modulus, zero-shear activation energy and flow recovery of the blend systems increase with the increase of Pluronic F127 content. There is a crossing point for the loss modulus and the storage modulus of each sample at high frequency, which is called specified frequency （SF）. The loss modulus is larger than the storage modulus when the frequency is less than the SF, and when frequency is more than SF, the loss modulus is smaller than the storage modulus.

Electrokinetic phenomena of poly(vinyl butyral) hollow fiber membranes in different electrolyte solutions

The streaming potential of poly（vinyl butyral） （PVB） hollow fiber membrane was studied in different electrolyte solutions （including NaCl, KCl, CaCl2 and MgCl2）, the effects of ionic strength, ion valence and pH value on the streaming potential （SP） of the membrane were investigated. The zeta potentials and surface charge densities of the membrane were estimated on the basis of Helmholtz-Smoluchowski equation and Gouy-Chapmann theory. The results show that the PVB membrane has a weak negative charge due to the specific adsorption of ions. Moreover, the streaming potential, the zeta potential and the surface charge density of the membrane depend strongly on the salt concentration and the type and valence of ions. The iso-electric point （IEP） of the PVB membrane is arotmd 3.0 in the monovalent media （NaC1 and KC1） and 3.5 in divalent electrolytes （CaCl2 and MgCl2）. A few retentions were obtained for PVB membrane in low concentration solutions. This result verifies that the negative charged membrane surface can reject inorganic solutes by means of electrostatic repulsion effect even though the size of membrane pores is much larger than the size of salts.

Sodium butyrate alleviates fructose-induced non-alcoholic fatty liver disease by remodeling gut microbiota to promoteγ-amino butyric acid production

Sodium butyrate(NaB)can regulate lipid metabolism and inhibit hepatic steatosis.This study aimed to investigate whether NaB can alleviate fructose-induced hepat ic steatosis via remodeling the gut microbiota and evaluate the anti-fatty liver mechanisms.The results showed that NaB and NaB-remodeled gut microbiota significantly alleviated fructose-induced hepatic steatosis and increased plasma uric acid and fructose levels.Furthermore,both NaB and NaB-remodeled gut microbiota increased the abundance of Lactobacillus and altered the levels of plasma amino acids(upregulating gamma-amino butyric acid(GABA)and downregulating L-glutamic acid and L-arginine)in fructose-exposed mice.The correlation analysis showed that GABA levels positively correlated with Lactobacillus abundance,and increased GABA levels might promote the reduction of the hepatic triglyceride content.Further studies confirmed that GABA significantly reduced lipid deposition in mouse hepatocytes induced via fructose pretreatment in vitro.These findings suggested that NaB could ameliorate fructose-induced hepatic steatosis by regulating gut microbiota.

Alginate oligosaccharide-mediated butyrate-HIF-1α axis improves skin aging in mice

The“gut-skin”axis has been proved and is considered as a novel therapy for the prevention of skin aging.The antioxidant efficacy of oligomannonic acid(MAOS)makes it an intriguing target for use to improve skin aging.The present study further explored whereby MAOS-mediated gut-skin axis balance prevented skin aging in mice.The data indicated the skin aging phenotypes,oxidative stress,skin mitochondrial dysfunction,and intestinal dysbiosis(especially the butyrate and HIF-1a levels decreased)in aging mice.Similarly,fecal microbiota transplantation(FMT)from aging mice rebuild the aging-like phenotypes.Further,we demonstrated MAOS-mediated colonic butyrate-HIF-1a axis homeostasis promoted the entry of butyrate into the skin,upregulated mitophagy level and ultimately improving skin aging via HDAC3/PHD/HIF-1a/mitophagy loop in skin of mice.Overall,our study offered a better insights of the effectiveness of alginate oligosaccharides(AOS),promised to become a personalized targeted therapeutic agents,on gut-skin axis disorder inducing skin aging.

Coated sodium butyrate ameliorates high‑energy and low‑protein diet induced hepatic dysfunction via modulating mitochondrial dynamics, autophagy and apoptosis in laying hens

Background Fatty liver hemorrhagic syndrome(FLHS),a fatty liver disease in laying hens,poses a grave threat to the layer industry,stemming from its ability to trigger an alarming plummet in egg production and usher in acute mortality among laying hens.Increasing evidence suggests that the onset and progression of fatty liver was closely related to mitochondria dysfunction.Sodium butyrate was demonstrated to modulate hepatic lipid metabolism,alle-viate oxidative stress and improve mitochondrial dysfunction in vitro and mice models.Nevertheless,there is limited existing research on coated sodium butyrate(CSB)to prevent FLHS in laying hens,and whether and how CSB exerts the anti-FLHS effect still needs to be explored.In this experiment,the FLHS model was induced by administering a high-energy low-protein(HELP)diet in laying hens.The objective was to investigate the effects of CSB on alleviating FLHS with a focus on the role of CSB in modulating mitochondrial function.Methods A total of 288 healthy 28-week-old Huafeng laying hens were arbitrarily allocated into 4 groups with 6 replicates each,namely,the CON group(normal diet),HELP group(HELP diet),CH500 group(500 mg/kg CSB added to HELP diet)and CH750 group(750 mg/kg CSB added to HELP diet).The duration of the trial encompassed a period of 10 weeks.Results The result revealed that CSB ameliorated the HELP-induced FLHS by improving hepatic steatosis and patho-logical damage,reducing the gene levels of fatty acid synthesis,and promoting the mRNA levels of key enzymes of fatty acid catabolism.CSB reduced oxidative stress induced by the HELP diet,upregulated the activity of GSH-Px and SOD,and decreased the content of MDA and ROS.CSB also mitigated the HELP diet-induced inflammatory response by blocking TNF-α,IL-1β,and F4/80.In addition,dietary CSB supplementation attenuated HELP-induced activation of the mitochondrial unfolded protein response(UPRmt),mitochondrial damage,and decline of ATPase activity.HELP diet decreased the autophagosome formation,and downregulated LC3B but upregulated p62 protein expression,which CSB administration reversed.CSB reduced HELP-induced apoptosis,as indicated by decreases in the Bax/Bcl-2,Caspase-9,Caspase-3,and Cyt C expression levels.Conclusions Dietary CSB could ameliorate HELP diet-induced hepatic dysfunction via modulating mitochondrial dynamics,autophagy,and apoptosis in laying hens.Consequently,CSB,as a feed additive,exhibited the capacity to prevent FLHS by modulating autophagy and lipid metabolism.

Fusobacterium nucleatum-induced imbalance in microbiome-derived butyric acid levels promotes the occurrence and development of colorectal cancer

BACKGROUND Colorectal cancer(CRC)ranks among the most prevalent malignant tumors globally.Recent reports suggest that Fusobacterium nucleatum(F.nucleatum)contributes to the initiation,progression,and prognosis of CRC.Butyrate,a short-chain fatty acid derived from the bacterial fermentation of soluble dietary fiber,is known to inhibit various cancers.This study is designed to explore whether F.nucleatum influences the onset and progression of CRC by impacting the intestinal metabolite butyric acid.AIM To investigate the mechanism by which F.nucleatum affects CRC occurrence and development.METHODS Alterations in the gut microbiota of BALB/c mice were observed following the oral administration of F.nucleatum.Additionally,DLD-1 and HCT116 cell lines were exposed to sodium butyrate(NaB)and F.nucleatum in vitro to examine the effects on proliferative proteins and mitochondrial function.RESULTS Our research indicates that the prevalence of F.nucleatum in fecal samples from CRC patients is significantly greater than in healthy counterparts,while the prevalence of butyrate-producing bacteria is notably lower.In mice colonized with F.nucleatum,the population of butyrate-producing bacteria decreased,resulting in altered levels of butyric acid,a key intestinal metabolite of butyrate.Exposure to NaB can impair mitochondrial morphology and diminish mitochondrial membrane potential in DLD-1 and HCT116 CRC cells.Consequently,this leads to modulated production of adenosine triphosphate and reactive oxygen species,thereby inhibiting cancer cell prolif-eration.Additionally,NaB triggers the adenosine monophosphate-activated protein kinase(AMPK)signaling pathway,blocks the cell cycle in HCT116 and DLD-1 cells,and curtails the proliferation of CRC cells.The combined presence of F.nucleatum and NaB attenuated the effects of the latter.By employing small interfering RNA to suppress AMPK,it was demonstrated that AMPK is essential for NaB’s inhibition of CRC cell proliferation.CONCLUSION F.nucleatum can promote cancer progression through its inhibitory effect on butyric acid,via the AMPK signaling pathway.

Effects of β-Amino Butyric Acid Induced Rice Blast Resistance on Reactive Oxygen Metabolism

[Objective] This study was to understand the effects of β-Amino butyric acid(abbreviated as BABA) induced rice blast resistance on reactive oxygen metabolism. [Method] Using the cultivar Chaochan 2 that is highly susceptible to disease as experimental material, the changes of catalase(CAT), and superoxide dismutase(SOD) and MDA activities in rice treated by BABA were investigated. [Result] In rice plants treated by BABA, the activities of CAT and SOD increased, meanwhile the MDA content also rose to some extent, resulting in the disease resistance to rice blast. [Conclusion] By influencing reactive oxygen metabolism, BABA endows rice plants with resistance to rice blast. BABA is safe to environment and has highly resistance-inducing capacity, it could be generalized in production.

Short communication Catalytic synthesis of butyric esters with TiSiW_(12)O_(40)/TiO_2

The catalytic activities of TiSiW_(12)O_(40)/TiO_2 in synthesizing ethylester; propyl ester, n-butyl ester; and amyl ester were reported. It was demonstrated thatTiSiW_(12)O_(40)/TiO_2 is an excellent catalyst. Various factors concerned with esterification wereinvestigated. The optimum conditions were found: the mole ratio of alcohol to acid is 1.3:1, themass ratio of catalyst to reactants is 1.5 percent, and the reaction time is 1.0 h. Under theoptimum conditions, the yields are 88.0 percent for ethyl ester, 94.5 percent for propyl ester, 98.6percent for n-butyl ester, 99.1 percent for n-amyl ester, and 96.7 percent for iso-amyl ester,respectively.

CREB-binding protein, p300, butyrate, and Wnt signaling in colorectal cancer

This paper reviews the distinctive roles played by the transcriptional coactivators CREB-binding protein(CBP) and p300 in Wnt/β-catenin signaling and cell physiology in colorectal cancer(CRC). Specifically, we focus on the effects of CBP- and p300-mediated Wnt activity on(1) neoplastic progression;(2) the activities of butyrate, a breakdown product of dietary fiber, on cell signaling and colonic cell physiology;(3) the development of resistance to histone deacetylase inhibitors(HDACis), including butyrate and synthetic HDACis, in colonic cells; and(4) the physiology and number of cancer stem cells. Mutations of the Wnt/β-catenin signaling pathway initiate the majority of CRC cases, and we have shown that hyperactivation of this pathway by butyrate and other HDACis promotes CRC cell apoptosis. This activity by butyrate may in part explain the preventive action of fiber against CRC. However, individuals with a high-fiber diet may still develop neoplasia; therefore, resistance to the chemopreventive action of butyrate likely contributes to CRC. CBP or p300 may modify the ability of butyrate to influence colonic cell physiology since the two transcriptional coactivators affect Wnt signaling, and likely, its hyperactivation by butyrate. Also, CBP and p300 likely affect colonic tumorigenesis, as well as stem cell pluripotency. Improvement of CRC prevention and therapy requires a better understanding of the alterations in Wnt signaling and gene expression that underlie neoplastic progression, stem cell fate, and the development of resistance to butyrate and clinically relevant HDACis. Detailed knowledge of how CBP- and p300 modulate colonic cell physiology may lead to new approaches for anti-CRC prevention and therapeutics, particularly with respect to combinatorial therapy of CBP/p300 inhibitors with HDACis.

响应面分析法优化一株窖泥源酪丁酸梭菌（Clostridium tyrobutyricum）RL1菌株产丁酸发酵培养基

从某浓香型白酒窖泥中筛选出1 株高产丁酸的酪丁酸梭菌(Clostridium tyrobutyricum)RL1 菌株,采用响应面分析法对其产丁酸培养基进行优化研究。首先采用Plackett-Burman 设计对基础培养基中9 个主要因素进行筛选,确定出对丁酸产量影响显著的3 个因素,依次为葡萄糖、碳酸钙和蛋白胨。对上述显著因素利用最陡爬坡试验逼近最大产酸响应区域,最后通过Box-Behnken 设计及响应面分析确定最佳培养基总成分组成为:葡萄糖85.29 g/L,酵母粉7.5 g/L,蛋白胨9.37 g/L,氯化钠7.5 g/L,乙酸钠4.5 g/L,磷酸氢二钾2.5 g/L,七水合硫酸镁0.3 g/L,硫酸铵1.5 g/L,七水合硫酸亚铁0.015 g/L,硫代乙醇酸钠0.5 g/L,碳酸钙11.6 g/L。优化后培养基的丁酸浓度为22.96 g/L,较优化前的14.23 g/L提高了61.35 %。

Beneficial effect of butyrate, Lactobacillus casei and L-carnitine combination in preference to each in experimental colitis

AIM: To investigate the beneficial effect of the combination of butyrate, Lactobacillus casei, and L-carnitine in a rat colitis model.

Sodium Butyrate Induces Apoptosis of Human Colon Cancer Cells by Modulating ERK and Sphingosine Kinase 2

Objective To investigate the role of extracellular signal-regulated kinase （ERK） in apoptosis of human colon cancer （HCT116） cells. Methods After the HCT116 cells were pretreated with specific ERK inhibitor （U0126） or specific siRNA and exposed to 10 mmol/L sodium butyrate （NaBT） for 24 h, their apoptosis was detected by flow cytometry, levels of SphK2 and ERK protein were measured by Western blot, and translocation of SphK2 was assayed by immunofluorescence microscopy. Results The U0126 and siRNAs specific for SphK2 blocked the export of SphK2 from nuclei to cytoplasm and increased the apoptosis of HCT116 cells following NaBT exposure. Over-expression of PKD decreased NaBT-induced apoptosis of HCT116 cells, which was reversed by U0126. Furthermore, transfection of HCT116 cells with constitutively activated PKD plasmids recovered the UO126-blocked export of SphK2. Conclusion ERK regulates the export of SphK2 and apoptosis of HCT116 cells by modulating PKD. Modulation of these molecules may help increase the sensitivity of colon cancer cells to the physiologic anti-colon cancer agent, NaBT.

Sodium butyrate prevents radiation-induced cognitive impairment by restoring pCREB/BDNF expression

Sodium butyrate is a histone deacetylase inhibitor that affects various types of brain damages.To investigate the effects of sodium butyrate on hippocampal dysfunction that occurs after whole-brain irradiation in animal models and the effect of sodium butyrate on radiation exposure-induced cognitive impairments,adult C57BL/6 mice were intraperitoneally treated with 0.6 g/kg sodium butyrate before exposure to 10 Gy cranial irradiation.Cognitive impairment in adult C57BL/6 mice was evaluated via an object recognition test 30 days after irradiation.We also detected the expression levels of neurogenic cell markers(doublecortin)and phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor.Radiation-exposed mice had decreased cognitive function and hippocampal doublecortin and phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor expression.Sodium butyrate pretreatment reversed these changes.These findings suggest that sodium butyrate can improve radiation-induced cognitive dysfunction through inhibiting the decrease in hippocampal phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor expression.The study procedures were approved by the Institutional Animal Care and Use Committee of Korea Institute of Radiological Medical Sciences(approval No.KIRAMS16-0002)on December 30,2016.

Promotion and Inhibition of Ruminal Epithelium Growth by Butyric Acid and Insulin-Like Growth Factor-1(IGF-1) in Dairy Goats

Isolated ruminal epithelia from caudal blind sacs of dairy goats were incubated with butyrate and insulin-like growth factor-1（IGF-1） at different concentrations. Proportions of ruminal epithelium in different phases of the cell division cycle were determined by flow cytometric analysis. The proportion of epithelial cells in S phase and G2-M phase（PS＆G2-M） increased significantly（P〈0.01） whereas the proportion of epithelial cells in G0-G1 phase（PG0-G1） decreased after incubation with IGF-1. PS＆G2-M decreased whereas PG0-G1 increased markedly（P〈0.01） after incubation with sodium butyrate. PS＆G2-M incubated with IGF-1 and butyrate sodium together increased more than that incubated with IGF-1 alone; PG0-G1, however, decreased significantly（P〈0.01）. Our results indicate that IGF-1 enhances whereas sodium butyrate inhibits the proliferation of rumen epithelial cells. Furthermore, butyrate and IGF-1, together, have a synergic effect on the proliferation of rumen epithelium.

Sodium butyrate attenuates high-fat diet-induced steatohepatitis in mice by improving gut microbiota and gastrointestinal barrier

AIM To investigate whether gut microbiota metabolite sodium butyrate (NaB) is an effective substance for attenuating non-alcoholic fatty liver disease (NAFLD) and the internal mechanisms. METHODS Male C57BL/6J mice were divided into three groups, normal control were fed standard chow and model group were fed a high-fat diet (HFD) for 16 wk, the intervention group were fed HFD for 16 wk and treated with NaB for 8 wk. Gut microbiota from each group were detected at baseline and at 16 wk, liver histology were evaluated and gastrointestinal barrier indicator such as zonula occluden-1 (ZO-1) were detected by immunohistochemistry and realtime-PCR, further serum or liver endotoxin were determined by ELISA and inflammation-or metabolism-associated genes were quantified by real-time PCR. RESULTS NaB corrected the HFD-induced gut microbiota imbalance in mice, while it considerably elevated the abundances of the beneficial bacteria Christensenellaceae, Blautia and Lactobacillus. These bacteria can produce butyric acid in what seems like a virtuous circle. And butyrate restored HFD induced intestinal mucosa damage, increased the expression of ZO-1 in small intestine, further decreased the levels of gut endotoxin in serum and liver compared with HF group. Endotoxin-associated genes such as TLR4 and Myd88, pro-inflammation genes such as MCP-1, TNF-alpha, IL-1, IL-2, IL-6 and IFN-gamma in liver or epididymal fat were obviously downregulated after NaB intervention. Liver inflammation and fat accumulation were ameliorated, the levels of TG and cholesterol in liver were decreased after NaB intervention, NAS score was significantly decreased, metabolic indices such as FBG and HOMA-IR and liver function indicators ALT and AST were improved compared with HF group. CONCLUSION NaB may restore the dysbiosis of gut microbiota to attenuate steatohepatitis, which is suggested to be a potential gut microbiota modulator and therapeutic substance for NAFLD.

Suppression of fibrosis in human pterygium fibroblasts by butyrate and phenylbutyrate

AIM：To evaluate the antifibrogenic effects of butyrate or phenylbutyrate,a chemical derivative of butyrate,in human pterygium fibroblasts.METHODS：Human pterygium fibroblasts obtained from patient pterygium tissue were treated with butyrate or phenylbutyrate for 48h.Expression ofα-smooth muscle actin,collagen I,collagen III and matrix metalloproteinase-1m RNA was measured by quantitative real-time reverse transcription polymerase chain reaction,and acetylated histone was evaluated by Western blotting.RESULTS：Butyrate inhibitedα-smooth muscle actin,type III collagen and matrix metalloproteinase-1 expressions,and phenylbutyrate inhibited types I and III collagen and matrix metalloproteinase-1 expressions without changing cell viability as well as both of these increased histone acetylation.These results suggested that butyrate and phenylbutyrate suppress fibrosis through a mechanism involving histone deacetylase inhibitor.CONCLUSION：This indicates that butyrate or phenylbutyrate have antifibrogenic effects in human pterygium fibroblasts and could be novel types of prophylactic and/or therapeutic drugs for pterygium,especially phenylbutyrate,which does not have the unpleasant smell associated with butyrate.

Effects of tachyplesin and n-sodium butyrate on proliferation and gene expression of human gastric adenocarcinoma cell line BGC-823

AIM： To investigate the effects of tachyplesin and n-sodium butyrate on proliferation and gene expression of human gastric adenocarcinoma cell line BGC-823. METHODS： Effects of tachyplesin and n-sodium butyrate on proliferation of BGC-823 cells were determined with trypan blue dye exclusion test and HE staining. Effects of tachyplesin and n-sodium butyrate on cell cycle were detected by flow cytometry. Protein levels of c-erbB-2, c-myc, p53 and p16 were examined by immunocytochemistry. RESULTS： The inhibiting effects were similar after 2.0 mg/L tachyplesin and 2.0 mmol/L n-sodium butyrate treatment, the inhibitory rate of cellular growth was 62.66% and 60.19% respectively, and the respective maximum mitotic index was decreased by 49.35% and 51.69% respectively. Tachyplesin and n-sodium buD/rate treatment could markedly increase the proportion of cells at G0/G1 phase and decrease the proportion at S phase. The expression levels of oncogene c-erbB-2, c-myc, and mtp53 proteins were down-regulated while the expression level of tumor suppressor gene p16 protein was up-regulated after the treatment with tachyplesin or n-sodium buD/rate. The effects of 1.0 mg/L tachyplesin in combination with 1.0 mmol/L n-sodium butyrate were obviously superior to their individual treatment in changing cell cycle distribution and expression of c-erbB-2, c-myc, mtp53 and p16 protein. The inhibitory rate of cellular growth of BGC-823 cells after combination treatment was 62.29% and the maximum mitotic index wasdecreased by 51.95%. CONCLUSION： Tachyplesin as a differentiation inducer of tumor cells has similar effects as n-sodium butyrate on proliferation of tumor cells, expression of correlative oncogene and tumor suppressor gene. It also has a synergistic effect on differentiation of tumor cells.