神经元缺氧复氧损伤时氧自由基的毒性作用及其机制

在原代分离培养Ｗｉｓｔａｒ乳鼠大脑皮质神经元上研究了缺氧复氧损伤（Ｈ／Ｒ）对神经细胞乳酸脱氢酶（ＬＤＨ）,漏出率,死亡率和脂质过氧化物含量的影响,并选用一氧化氮（ＮＯ）合酶抑制剂Ｌ－ＮＧ－硝基－精氨酸（Ｌ－ＮＮＡ）巯基供体Ｎ－乙酰半胱氨酸（ＮＡＣ）和超氧化物歧化酶（Ｃｕ,Ｚｎ－ＳＯＤ）三种自由基清除剂进行预保护等方法来探讨机制。结果表明 Ｈ／Ｒ损伤引起ＬＤＨ漏出率,细胞死亡率和脂过氧化物含量极显著     

神经元缺氧复氧损伤时氧自由基的毒性作用及其机制＊

在原代分离培养Ｗｉｓｔａｒ乳鼠大脑皮质神经元上研究了缺氧复氧损伤（Ｈ／Ｒ）对神经细胞乳酸脱氢酶（ＬＤＨ）,漏出率,死亡率和脂质过氧化物含量的影响,并选用一氧化氮（ＮＯ）合酶抑制剂Ｌ－ＮＧ－硝基－精氨酸（Ｌ－ＮＮＡ）巯基供体Ｎ－乙酰半胱氨酸（ＮＡＣ）和超氧化物歧化酶（Ｃｕ,Ｚｎ－ＳＯＤ）三种自由基清除剂进行预保护等方法来探讨机制。结果表明 Ｈ／Ｒ损伤引起ＬＤＨ漏出率,细胞死亡率和脂过氧化物含量极显著     

缺氧预处理对乳鼠心肌细胞蛋白激酶C活性的影响

在培养的乳鼠心肌细胞缺氧／复氧模型上,观察了缺氧预处理的细胞保护作用及其对细胞蛋白激酶Ｃ活性和蛋白磷酸化的影响。结果表明,ＡＰＣ可减轻心肌细胞的Ｈ／Ｒ损伤;提高细胞存活率,减少细胞脂质过氧化产物生成及细胞内乳酸脱氢酶和蛋白质漏出。模拟ＡＰＣ的短暂缺氧显著激活ＰＫＣ,使心肌细胞内分子量为６６ｋＤ和３１ｋＤ的蛋白条带＾３２Ｐ掺入增加;ＰＫＣ抑制剂Ｈ７完全消除ＡＰＣ对心肌细胞的保护作用,并抑制了短暂缺氧     

碱性成纤维细胞生长因子对乳鼠心肌细胞缺氧复氧损伤的影响

本实验在培养的乳鼠心肌细胞缺氧复氧损伤模型上观察碱性纤维细胞生长因子对Ａ／Ｒ损伤及蛋白激酶活性的影响,以探讨ｂＥＧＦ作为药物预处理心肌保护的可行性及其机理。结果表明,ｂＥＧＦ预处理呈浓度依赖地提高Ａ／Ｒ后心肌细胞存活率,减少细胞内ＡＴＰ消耗及胞浆乳酸脱氢酶漏出;ＰＫＣ抑制剂Ｈ７完全消除ｇＦＧＦ的上述保护作用;实验结果表明,ｂＦＧＦ可以直接激活心肌细胞ＰＫＣ,其激活时相的变化与缺氧预处理者相近,提示     

生长抑素对羟自由基损伤的人胃粘膜上皮细胞系GES—1的影响

目的和方法：采用人胃粘膜上皮细胞系ＧＥＳ１细胞传代培养技术,利用Ｆｅ２＋与Ｈ２Ｏ２反应生成的羟自由基（ｈｙｄｒｏｘｙｌｒａｄｉｃａｌ,ＯＨ·）建立细胞损伤模型,探讨ＯＨ·损伤人胃粘膜细胞的机制,观察生长抑素（ｓｏｍａｔｏｓｔａｔｉｎ,ＳＳ）对ＧＥＳ１细胞抗ＯＨ·损伤的影响。结果：（１）ＯＨ·可直接损伤ＧＥＳ１细胞,表现为细胞存活率下降而细胞乳酸脱氢酶（ｌａｃｔａｔｅｄｅｈｙｄｒｏｇｅｎａｓｅ,ＬＤＨ）漏出量增多;预先在细胞培养液中加入ＯＨ·特异性清除剂二甲基亚砜（５ｍｍｏｌ／Ｌ）,可预防该损伤。预先加入ＳＳ（０．０１ｍｇ／Ｌ,０．１ｍｇ／Ｌ,１．０ｍｇ／Ｌ,１０ｍｇ／Ｌ）对细胞存活率和细胞ＬＤＨ漏出量无影响;（２）加入ＯＨ·后,细胞丙二醛（ＭＤＡ）、氧化型谷胱甘肽（ＧＳＳＧ）含量上升而还原型谷胱甘肽（ＧＳＨ）含量下降。以ＳＳ０．１ｍｇ／Ｌ,１．０ｍｇ／Ｌ,１０ｍｇ／Ｌ预处理,可部分减轻上述改变。结论：ＯＨ·可直接损伤ＧＥＳ１细胞,其机制与破坏细胞的巯基稳态及加重细胞的脂质过氧化程度有关;ＳＳ可通过维持细胞的巯基稳态,部分减轻ＯＨ·所致的ＧＥＳ１细胞脂质过氧化程度。     

肝细胞生长因子对四氯化碳损伤肝细胞的保护作用及相关基因表达

利用无血清原代培养大鼠肝细胞,观察重组人肝细胞生长因子（ｒｈＨＧＦ）对ＣＣｌ４染毒肝细胞的保护作用。结果表明：（１）ｒｈＨＧＦ（５ｎｇ／ｍｌ）预自理后可显著提高ＣＣｌ４（１５ｍｍｏｌ／Ｌ）染毒肝细胞存活率,降低细胞内丙氨酸氨基转移酶（ＡＬＴ）、Ｋ＾＋的漏出;（２）表皮生长因子（ＥＧＦ,５０ｎｇ／ｍｌ）和ｒｈＨＧＦ（５ｎｇ／ｍｌ）合用预处理肝细胞,ＣＣｌ４染毒后细胞内ＡＬＴ、Ｋ＾＋漏出较ｒｈＨＧＦ和     

黑龙江铜木蚜蝇雌性的描述

黑龙江铜木蚜蝇雌性的描述ＤＥＳＣＲＩＰＴＩＯＮＯＦＴＨＥＦＥＭＡＬＥＣＨＡＬＣＯＳＹＲＰＨＵＳ（ＸＹＬＯＴＯＭＩＭＡ）ＡＭＵＲＥＮＳＩＳ（ＳＴＡＣＫＥＬＢＥＲＧ）（ＤＩＰＴＥＲＡ：ＳＹＲＰＨＩＤＡＥ）￥ＨＥＪｉｌｏｎｇ;ＣＨＵＸｉｐｉｎｇ（Ｄｅｐａｒ...     

血管活性肠肽对兔支气管上皮细胞抗臭氧损伤的保护作用

用支气管刷洗法收集新西兰兔支气管上皮细胞（ＢＥＣ）,以臭氧（Ｏ３）攻击培养的ＢＥＣ,建立细胞损伤模型。测定ＢＥＣ的３Ｈ释放率计算Ｏ３的细胞毒指数（ＣＩ）、测定细胞内丙二醛（ＭＤＡ）的含量反映细胞氧化性损伤的程度,测定细胞内过氧化氢酶（ＣＡＴ）活性及还原型和氧化型谷胱甘肽（ＧＳＨ和ＧＳＳＧ）的含量反映细胞抗氧化能力。观察血管活性肠肽（ＶＩＰ）预处理对ＢＥＣ的细胞保护作用并初步探讨其保护机制。观察到：ＢＥＣ的３Ｈ释放率与Ｏ３暴露时间成正比;Ｏ３暴露２ｈ使ＭＤＡ含量和ＧＳＳＧ含量明显增加,ＧＳＨ减少;ＶＩＰ预处理呈剂量依赖性降低Ｏ３暴露的ＣＩ值、降低ＭＤＡ和ＧＳＳＧ含量、增加ＧＳＨ及ＧＳＨ／ＧＳＳＧ比值、增加ＣＡＴ活性,显示出细胞保护效应;ＶＩＰ的保护效应可被放线菌素Ｄ（Ａ－Ｄ）或蛋白激酶Ｃ阻断剂Ｈ７部分取消。结果表明：Ｏ３暴露会导致ＢＥＣ损伤,ＶＩＰ可通过增强ＢＥＣ的抗氧化能力而保护ＢＥＣ,ＶＩＰ的信号在细胞内的转导途径与基因转录及依赖ＰＫＣ的酶蛋白磷酸化有关。     

铜对马铃薯块茎产量与生理生化特性的影响

铜对马铃薯块茎产量与生理生化特性的影响白嵩吕芳芝＊白宝璋李秀坤刘志清＊＊陈文荣（吉林农业大学,长春１３０１１８）ＥＦＦＥＣＴＳＯＦＣＯＰＰＥＲＯＮＴＵＢＥＲＹＩＥＬＤＡＮＤＰＨＹＳＩＯ┐ＬＯＧＩＣＡＬＡＮＤＢＩＯＣＨＥＭＩＣＡＬＣＨＡＲＡＣ┐ＴＥＲ...     

蛋白激酶C参与缺氧预处理的血管平滑肌细胞保护

已知缺氧预处理不仅对心肌细胞,而且对血管床亦有保护作用;但对血管壁细胞是否有直接保护作用,目前尚不清楚。本工作在培养的家兔血管平滑肌细胞（ＶＳＭＣ）缺氧复氧（Ａ／Ｒ）损伤模型上观察缺氧预处理（ａｎｏｘｉｃｐｒｅｃｏｎｄｉｔｉｏｎｉｎｇ,ＡＰＣ）的影响。发现ＡＰＣ能提高Ａ／Ｒ后ＶＳＭＣ存活率,减轻细胞脂质过氧化损伤和钙超载,使用蛋白激酶Ｃ（ＰＫＣ）激动剂ＰＭＡ能模拟,而抑制剂Ｈ７或ｐｏｌｙｍｙｘｉｎＢ能完全消除ＡＰＣ的上述保护作用。提示ＡＰＣ对ＶＳＭＣ的Ａ／Ｒ损伤具有保护作用,其机理可能与ＰＫＣ激活有关     

Salvia miltiorrhiza attenuates the changes in contraction and intracellular calcium induced by anoxia and reoxygenation in rat cardiomyocytes

The aim of the present study is to investigate the effect of Salvia miltiorrhiza (SM) on contraction and the intracellular calcium of isolated ventricular myocytes during normoxia or anoxia and reoxygenation using a video tracking system and spectrofluorometry. Cardiac ventricular myocytes were isolated enzymatically by collagenase and exposed to 5 min of anoxia followed by 10 min of reoxygenation. SM (1-9 g/L) depressed both contraction and the [Ca(2+)](i) transient in a dose-dependent manner. SM did not affect the diastolic calcium level and the sarcolemmal Ca(2+) channel of myocytes but decreased the caffeine-induced calcium release. During anoxia, the +/-dL/dtmax, amplitudes of contraction (dL) of cell contraction and [Ca(2+)](i) transients were decreased, while the diastolic calcium level was increased. None of the parameters returned to the pre-anoxia level during reoxygenaton. However, SM (3 g/L) did attenuate the changes in cell contraction and intracellular calcium induced by anoxia and reoxygenation. It is concluded that SM has different effects on normoxic and anoxic cardiomyocytes. The SM-induced reduction of changes in contraction and intracellular calcium induced by anoxia/reoxygenation indicates that SM may be beneficial for cardiac tissue in recovery of mechanical function and intracellular calcium homeostasis.     

EGb 761 protects liver mitochondria against injury induced by in vitro anoxia/reoxygenation.

The present study investigated the protective effects of Ginkgo biloba extract (EGb 761) on rat liver mitochondrial damage induced by in vitro anoxia/reoxygenation. Anoxia/reoxygenation was known to impair respiratory activities and mitochondrial oxidative phosphorylation efficiency. ADP/O (2.57 +/- 0.11) decreased after anoxia/reoxygenation (1.75 +/- 0.09, p < .01), as well as state 3 and uncoupled respiration (-20%, p < .01), but state 4 respiration increased (p < .01). EGb 761 (50-200 microg/ml) had no effect on mitochondrial functions before anoxia, but had a specific dose-dependent protective effect after anoxia/reoxygenation. When mitochondria were incubated with 200 microg/ml EGb 761, they showed an increase in ADP/O (2.09 +/- 0.14, p < .05) and a decrease in state 4 respiration (-22%) after anoxia/reoxygenation. In EPR spin-trapping measurement, EGb 761 decreased the EPR signal of superoxide anion produced during reoxygenation. In conclusion, EGb 761 specially protects mitochondrial ATP synthesis against anoxia/reoxygenation injury by scavenging the superoxide anion generated by mitochondria.     

Oxygen radicals generated during anoxia followed by reoxygenation reduce the synthesis of tissue-type plasminogen activator and plasminogen activator inhibitor-1 in human endothelial cell culture

The effect of anoxia and reoxygenation on the synthesis and secretion of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) was studied in primary cultures of human umbilical vein endothelial cells. Sublethal anoxia, determined by trypan blue dye exclusion and lactate dehydrogenase release, was produced by cell culture under a 95% N2, 5% CO2 atmosphere for 2-24 h and was followed by reoxygenation with 95% air, 5% CO2 for 24 or 48 h. Anoxia did not alter the levels of mRNA for t-PA or PAI-1 in the cells or the secretion of t-PA or PAI-1 into the medium. At 24 h, t-PA secreted into conditioned medium was 7.0 +/- 1.4 ng/2 x 10(6) cells (n = 9) and PAI-1 was 300 +/- 13 IU/2 x 10(6) cells (n = 9), whereas the content of t-PA mRNA was 2.2 pg/micrograms of RNA and PAI-1 mRNA was 180 pg/micrograms of RNA. During reoxygenation, however, t-PA antigen and PAI-1 activity as well as mRNA for PAI-1 decreased proportionally to the duration of anoxia, to reach 27 +/- 1.0, 49 +/- 2.0, and 47 +/- 14% of control values, respectively, within 24 h of anoxia. t-PA mRNA also decreased significantly during reoxygenation following anoxia, but the extent could not be accurately quantitated. Addition, during anoxia, of a 200 micrograms/ml concentration of the superoxide anion radical scavenger superoxide dismutase or of a 5 mM concentration of the iron chelator deferoxamine mesylate prevented the subsequent decrease of t-PA antigen during reoxygenation; addition of these compounds during reoxygenation had no effect. Superoxide dismutase, but not deferoxamine mesylate, when added during anoxia prevented the subsequent decrease in PAI-1 activity. These studies suggest that the marked alteration of endothelial cell fibrinolysis during anoxia followed by reoxygenation is most likely mediated by a mechanism dependent on oxygen radicals. Impaired endothelial cell fibrinolysis may contribute to the pathophysiology of ischemia/reperfusion injury.     

Glutamine supports recovery from loss of transepithelial resistance and increase of permeability induced by media change in Caco-2 cells

Recent evidence suggests that the conditionally essential amino acid glutamine is important for intestinal barrier function. However, the mechanism remains undefined. To determine the effects of glutamine on permeability of intestinal epithelial cell monolayers, Caco-2 cells were grown on membrane filters and exposed to 4 mmol/L sodium butyrate in order to rapidly achieve high levels of alkaline phosphatase and high transepithelial resistance as seen in functionally mature enterocytes. A standard method of medium exchange consisting of removal and replacement resulted in a catastrophic loss of transepithelial resistance and increase of mannitol and dextran fluxes that required 2-4 hrs and protein synthesis to recover. The effect was attributed to exposure of the upper monolayer surface to atmosphere and could be avoided by refeeding by incremental perfusion. Spontaneously-differentiated Caco-2 monolayers were resistant to this stress. This novel stress test was employed as a sensitive assay for the requirement of glutamine for monolayer transepithelial resistance and mannitol permeability. Pre-stress glutamine availability was more important than Gln-availability during the recovery phase. Thus the transepithelial resistance and permeability of butyrate-induced monolayers is dynamically-regulated in response to atmospheric exposure, by a mechanism that depends on threshold levels of glutamine availability.     

Resistance of isolated pulmonary mitochondria during in vitro anoxia/reoxygenation

The aim of the study was to investigate the effect of in vitro anoxia/reoxygenation on the oxidative phosphorylation of isolated lung mitochondria. Mitochondria were isolated after harvesting from fresh pig lungs flushed with Euro-Collins solution. Mitochondrial respiratory parameters were determined in isolated mitochondria before anoxia (control), after 5-45 min anoxia followed by 5 min reoxygenation, and after 25 or 40 min of in vitro incubation in order to follow the in vitro aging of mitochondria during respiratory assays. Respiratory parameters measured after anoxia/reoxygenation did not show any oxidative phosphorylation dysfunction, indicating a high resistance of pulmonary mitochondria to in vitro anoxia/reoxygenation (up to 45 min anoxia). These results indicate that mitochondria are not directly responsible of their oxidative phosphorylation damage observed after in vivo ischemia (K. Willet et al., Transplantation 69 (2000) 582) but are a target of others cellular injuries leading to mitochondrial dysfunction in vivo.     

谷氨酰胺对微囊化重组CHO细胞生长代谢及内皮抑素表达的影响

微囊化技术是一种有发展潜力的生物技术,在细胞移植和药物控释等方面具有广泛的应用。然而由于目前微囊化细胞规模化培养技术还不成熟,阻碍了其在临床治疗中的推广与应用。为了了解微囊化重组CHO细胞的生长代谢特性为今后规模化培养优化提供技术参考,考察了主要氮源物质谷氨酰胺对微囊化重组CHO细胞生长代谢及内皮抑素表达的影响。结果显示:当谷氨酰胺起始浓度从2.69mmolL增加到9.05mmolL时最大活细胞密度并没有增高,细胞增殖没有显著差异。当谷氨酰胺起始浓度较低(2.69mmolL)时,葡萄糖的比消耗速率较大;当谷氨酰胺起始浓度增高时(7.91mmolL～9.05mmolL)葡萄糖和谷氨酰胺的比消耗速率增大,但细胞对葡萄糖和谷氨酰胺的利用率降低。谷氨酰胺对产物表达有显著影响,起始浓度为4.97mmolL时的内皮抑素累积浓度最高,达546.36ngmL,过低和过高谷氨酰胺起始浓度下内皮抑素的累积浓度均较低。     

Lactobacillus casei DN-114 001 inhibits the ability of adherent-invasive Escherichia coli isolated from Crohn's disease patients to adhere to and to invade intestinal epithelial cells

Ileal lesions in 36.4% of patients with Crohn's disease are colonized by pathogenic adherent-invasive Escherichia coli. The aim of this study was to determine the in vitro inhibitory effects of the probiotic strain, Lactobacillus casei DN-114 001, on adhesion to and invasion of human intestinal epithelial cells by adherent-invasive E. coli isolated from Crohn's disease patients. The experiments were performed with undifferentiated Intestine-407 cells and with undifferentiated or differentiated Caco-2 intestinal epithelial cells. Bacterial adhesion to and invasion of intestinal epithelial cells were assessed by counting CFU. The inhibitory effects of L. casei were determined after coincubation with adherent-invasive E. coli or after preincubation of intestinal cells with L. casei prior to infection with adherent-invasive E. coli. Inhibitory effects of L. casei on adherent-invasive E. coli adhesion to differentiated and undifferentiated intestinal epithelial cells reached 75% to 84% in coincubation and 43% to 62% in preincubation experiments, according to the cell lines used. Addition of L. casei culture supernatant to the incubation medium increased L. casei adhesion to intestinal epithelial cells and enhanced the inhibitory effects of L. casei. The inhibitory effects on E. coli invasion paralleled those on adhesion. This effect was not due to a bactericidal effect on adherent-invasive E. coli or to a cytotoxic effect on epithelial intestinal cells. As Lactobacillus casei DN-114 001 strongly inhibits interaction of adherent-invasive E. coli with intestinal epithelial cells, this finding suggests that the probiotic strain could be of therapeutic value in Crohn's disease.     

Molecular mechanisms contributing to glutamine-mediated intestinal cell survival

Glutamine, the most abundant amino acid in the bloodstream, is the preferred fuel source for enterocytes and plays a vital role in the maintenance of mucosal growth. The molecular mechanisms regulating the effects of glutamine on intestinal cell growth and survival are poorly understood. Here, we show that addition of glutamine (1 mmol/l) enhanced rat intestinal epithelial (RIE)-1 cell growth; conversely, glutamine deprivation increased apoptosis as noted by increased DNA fragmentation and caspase-3 activity. To delineate signaling pathways involved in the effects of glutamine on intestinal cells, we assessed activation of extracellular signal-related kinase (ERK), protein kinase D (PKD), and phosphatidylinositol 3-kinase (PI3K)/Akt, which are important pathways in cell growth and survival. Addition of glutamine activated ERK and PKD in RIE-1 cells after a period of glutamine starvation; inhibition of ERK, but not PKD, increased cell apoptosis. Conversely, glutamine starvation alone increased phosphorylated Akt; inhibition of Akt enhanced RIE-1 cell DNA fragmentation. The role of ERK was further delineated using RIE-1 cells stably transfected with an inducible Ras. Apoptosis was significantly increased following ERK inhibition, despite Ras activation. Taken together, these results identify a critical role for the ERK signaling pathways in glutamine-mediated intestinal homeostasis. Furthermore, activation of PI3K/Akt during periods of glutamine deprivation likely occurs as a protective mechanism to limit apoptosis associated with cellular stress. Importantly, our findings provide novel mechanistic insights into the antiapoptotic effects of glutamine in the intestine.     

Effects of azathioprine and its metabolites on repair mechanisms of the intestinal epithelium in vitro

Erosions and ulcerations of the intestinal epithelium are hallmarks of inflammatory bowel diseases (IBD). Intestinal epithelial cell migration (restitution) and proliferation are pivotal mechanisms for healing of epithelial defects after mucosal injury. In addition, the rate of apoptosis of epithelial cells may modulate intestinal wound healing. The purine antagonists azathioprine (AZA) and 6-mercaptopurine (6-MP) are widely used drugs in the treatment of IBD. In the present study, the hitherto unknown effects of AZA as well as its metabolites 6-MP and 6-thioguanine (6-TG) on repair mechanisms and apoptosis of intestinal epithelia were analysed. Intestinal epithelial cell lines (human Caco-2, T-84 and HT-29 cells, rat IEC-6 cells) were incubated with AZA, 6-MP or 6-TG for 24 h (final concentrations 0.1-10 microM). Migration of Caco-2 and IEC-6 cells was analysed by in vitro restitution assays. Caco-2 and IEC-6 cell proliferation was evaluated by measurement of [3H]thymidine incorporation into DNA. Apoptosis of Caco-2, T-84, HT-29 and IEC-6 cells was assessed by histone ELISA, 4'6'diamidino-2'phenylindole-dihydrochloride staining as well as flow cytometric analysis of Annexin V/propidium iodide (PI)-stained cells. Cell cycle progression was evaluated by PI staining and flow cytometry. Epithelial restitution was not significantly affected by any of the substances tested. However, proliferation of intestinal epithelial cells was inhibited in a dose-dependent manner (maximal effect 92%) by AZA, 6-MP as well as 6-TG. In HT-29 cells, purine antagonist-effected inhibition of cell proliferation was explained by a cell cycle arrest in the G2 phase. In contrast, AZA, 6-MP and 6-TG induced no cell cycle arrest in Caco-2, T-84 and IEC-6 cells. AZA, 6-MP as well as 6-TG induced apoptosis in the non-transformed IEC-6 cell line but not in human Caco-2, T-84 and HT-29 cells. In summary, AZA and its metabolites exert no significant effect on intestinal epithelial restitution. However, they profoundly inhibit intestinal epithelial cell growth via various mechanisms: they cause a G2 cell cycle arrest in HT-29 cells, induce apoptosis in IEC-6 cells and dose-dependently inhibit intestinal epithelial proliferation.     

Glycerol supplementation enhances L. reuteri's protective effect against S. Typhimurium colonization in a 3-D model of colonic epithelium

The probiotic effects of Lactobacillus reuteri have been speculated to partly depend on its capacity to produce the antimicrobial substance reuterin during the reduction of glycerol in the gut. In this study, the potential of this process to protect human intestinal epithelial cells against infection with Salmonella enterica serovar Typhimurium was investigated. We used a three-dimensional (3-D) organotypic model of human colonic epithelium that was previously validated and applied to study interactions between S. Typhimurium and the intestinal epithelium that lead to enteric salmonellosis. Using this model system, we show that L. reuteri protects the intestinal cells against the early stages of Salmonella infection and that this effect is significantly increased when L. reuteri is stimulated to produce reuterin from glycerol. More specifically, the reuterin-containing ferment of L. reuteri caused a reduction in Salmonella adherence and invasion (1 log unit), and intracellular survival (2 log units). In contrast, the L. reuteri ferment without reuterin stimulated growth of the intracellular Salmonella population with 1 log unit. The short-term exposure to reuterin or the reuterin-containing ferment had no observed negative impact on intestinal epithelial cell health. However, long-term exposure (24 h) induced a complete loss of cell-cell contact within the epithelial aggregates and compromised cell viability. Collectively, these results shed light on a potential role for reuterin in inhibiting Salmonella-induced intestinal infections and may support the combined application of glycerol and L. reuteri. While future in vitro and in vivo studies of reuterin on intestinal health should fine-tune our understanding of the mechanistic effects, in particular in the presence of a complex gut microbiota, this the first report of a reuterin effect on the enteric infection process in any mammalian cell type.