Sialic Acid Reduces Acute Endotoxemia-induced Liver Dysfunction in the Rat

Ho, Chien-hsing; Hsu, Su-Ping; Yanɡ, Chao; Lee, Yi-Huey; Chien, Chiang‐Ting

doi:10.1097/shk.0b013e318199453c

Cited by 2 publications

(3 citation statements)

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“…Endotoxemia caused by lipopolysaccharide (LPS) is marked by global activation of inflammatory responses, which can lead to shock and multiple organ failure (1,2).…”

Section: Introductionmentioning

confidence: 99%

HSF-1 is Involved in Attenuating the Release of Inflammatory Cytokines Induced by LPS Through Regulating Autophagy

Tong¹,

Jiang²,

Zhang³

et al. 2014

Shock

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Autophagy plays a protective role in endotoxemic mice. Heat shock factor 1 (HSF-1) also plays a crucial protective role in endotoxemic mice by decreasing inflammatory cytokines. The purpose of this study was to determine whether HSF-1 is involved in attenuating the release of inflammatory cytokines in lipopolysaccharide (LPS)-stimulated mice and peritoneal macrophages (PMs) through regulating autophagy activity. Autophagosome formation in HSF-1(+/+) and HSF-1(-/-) mice and PMs stimulated by LPS was examined by Western blotting and immunofluorescence. Lipopolysaccharide-induced autophagy and inflammatory cytokines were examined in HSF-1(+/+) and HSF-1(-/-) PMs treated with 3-methyladenine (3-MA) or rapamycin. Results showed that LPS-induced autophagy was elevated transiently at 12 h but declined at 24 h in the livers and lungs of mice. Higher levels of inflammatory cytokines and lower autophagy activity were detected in HSF-1(-/-) mice and PMs compared with HSF-1(+/+) mice and PMs. Interestingly, LPS-induced release of inflammatory cytokines did not further increase in HSF-1(-/-) PMs treated with 3-MA but aggravated in HSF-1(+/+) PMs. Lipopolysaccharide-induced autophagy did not decrease in HSF-1(-/-) PMs treated with 3-MA but decreased in HSF-1 PMs(+/+). Taken together, our results suggested that HSF-1 attenuated the release of inflammatory cytokines induced by LPS by regulating autophagy activity.

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“…Endotoxemia caused by lipopolysaccharide (LPS) is marked by global activation of inflammatory responses, which can lead to shock and multiple organ failure (1,2).…”

Section: Introductionmentioning

confidence: 99%

HSF-1 is Involved in Attenuating the Release of Inflammatory Cytokines Induced by LPS Through Regulating Autophagy

Tong¹,

Jiang²,

Zhang³

et al. 2014

Shock

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“…6 Adherence of influenza virus or H. pylori to the target cells involves the interaction of sialic acid-containing glycoproteins or glycolipids, which present opportunities for prevention of viral and bacterial intervention. 7,8 Exogenous sialic acids are instrumental in regulating biological processes either by inhibiting particular interactions through masking or by mediating the binding of carbohydrate binding proteins between target cell and pathogen. 8 On the other hand, green tea extracts containing the epimers (+)-catechin, (-)-epicatechin, (+)-gallocatechin, (-)-epigallocatechin, (-)-epicatechin gallate and (-)-epigallocatechin gallate are considered to be strong antioxidants and to exert protective effects against inflammatory and cardiovascular diseases.…”

Section: Please Scroll Down For Articlementioning

confidence: 99%

“…7,8 Exogenous sialic acids are instrumental in regulating biological processes either by inhibiting particular interactions through masking or by mediating the binding of carbohydrate binding proteins between target cell and pathogen. 8 On the other hand, green tea extracts containing the epimers (+)-catechin, (-)-epicatechin, (+)-gallocatechin, (-)-epigallocatechin, (-)-epicatechin gallate and (-)-epigallocatechin gallate are considered to be strong antioxidants and to exert protective effects against inflammatory and cardiovascular diseases. 9 Catechins can inhibit proinflammatory and proapoptotic oxidative injury via the action of reduction in ROS production, nuclear factor-κB and activated protein-1 translocation, and intercellular adhesion molecule 1 expression as well as other proapoptotic mechanisms.…”

Section: Please Scroll Down For Articlementioning

confidence: 99%

A new approach for the prevention and treatment ofHelicobacter pyloriinfection via upregulation of autophagy and downregulation of apoptosis

Yang

Chien

2009

Autophagy

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Helicobacter pylori infection plays a crucial role in the pathogenesis of peptic ulcer and gastric cancer. The current proton pump inhibitor-based triple regimens or second-line therapies for the eradication of Helicobacter pylori face an increase in resistance problems, demanding a search for novel candidates. A new strategy for reduction of Helicobacter pylori infection is to interfere with the interaction between bacteria and target cells and to kill the bacteria but not target cells at the same time. By this approach, we found that the combination of anti-adhesion, antibacterial, antioxidant agents like sialic acid and catechins have a protective potential against Helicobacter pylori-induced gastric injury via a biphasic response in apoptosis and autophagy. The combination of sialic acid and catechins induced an upregulation in autophagy and a downregulation in apoptosis in the Helicobacter pylori-infected gastric epithelium and efficiently reduced gastric inflammation. It appears that a novel agent or a combination of several agents can be utilized to protect against Helicobacter pylori-induced gastric injury via the mechanism of upregulation of survival-related autophagy and downregulation of death-related apoptosis.

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Sialic Acid Reduces Acute Endotoxemia-induced Liver Dysfunction in the Rat

Cited by 2 publications

References 0 publications

HSF-1 is Involved in Attenuating the Release of Inflammatory Cytokines Induced by LPS Through Regulating Autophagy

HSF-1 is Involved in Attenuating the Release of Inflammatory Cytokines Induced by LPS Through Regulating Autophagy

A new approach for the prevention and treatment ofHelicobacter pyloriinfection via upregulation of autophagy and downregulation of apoptosis

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