Protective effect of Ulinastatin against murine models of sepsis: Inhibition of TNF-α and IL-6 and augmentation of IL-10 and IL-13

Cao, Yangsen; Tu, Yanyang; Chen, Xiang; Wang, Boliang; Zhong, Yi; Liu, Minghua

doi:10.1016/j.etp.2010.11.011

Cited by 72 publications

(49 citation statements)

References 33 publications

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“…Thus it is very important to inhibit the release of TNF. In the recently years, study found out UTI may significantly reduce the level of TNF-to protect the tissue and organ during sepsis (Cao et al 2010). Also a Japanese research team verify above conclusion in the other side, they found out in the pathogenesis of postresuscitation syndrome, insufficient production of UTI for norepinephrine (NE) releasing, accompanied by persistent high TNF-levels (Hayakawa et al 2008).…”

Section: Inhibit Releasing Of Tnf-α To Act As Protective Actionmentioning

confidence: 85%

“…However, Park, J. H. et al (Park et al 2010a) found out UTI can reduce the level of stress reaction related cytokine such as IL-6 during gastrointestinal operation, also in the trauma patients with hemorrhagic shock has the similar discovery (Park et al 2010b). This function was also verified by the septic rat model (Cao et al 2010). Thus, UTI may regulate the level of IL-6 to act as anti-inflammatory role.…”

Section: Inhibit Releasing Of Il-6 To Act As Protective Actionmentioning

confidence: 98%

“…Kurt, A. N. et al (Kurt et al 2007) found out the level of serum IL-8 in the patients with positive blood culture was found elevated significantly more than negative ones. It was also reported that UTI, as a broad-spectrum anti-inflammatory substance, may significantly down-regulate the production of IL-8 (Cao et al 2010). Bae, H. B. et al (Bae et al 2011) discovered the level of IL-8 in the UTI preconditioning sepsis rats is significantly lower than those in sepsis rats without treatment, and associated pathological section, they hold the opinion that UTI may through inhibiting IL-8 and so on mediators of inflammation in septic rats to act as a protective role in the septic process.…”

Section: Inhibit Releasing Of Il-8 To Act As Protective Actionmentioning

confidence: 99%

See 2 more Smart Citations

Ulinastatin and Septic Cardiac Dysfunction

Lin¹,

Lin²

2012

The Transmission Electron Microscope

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Section: Inhibit Releasing Of Tnf-α To Act As Protective Actionmentioning

confidence: 85%

Section: Inhibit Releasing Of Il-6 To Act As Protective Actionmentioning

confidence: 98%

Section: Inhibit Releasing Of Il-8 To Act As Protective Actionmentioning

confidence: 99%

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Ulinastatin and Septic Cardiac Dysfunction

Lin¹,

Lin²

2012

The Transmission Electron Microscope

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“…The increased production of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 has been implicated in the development of sepsis, and contributes to tissue damage and increased inflammatory response (Cao et al, 2012;Li et al, 2013;Yang et al, 2009;Zou et al, 2013). TNF-α, a pro-inflammatory cytokine, is considered an important mediator in inflammation, and is present in the serum of animals and humans undergoing sepsis (O´Callaghan and Redmond, 2006).…”

Section: Discussionmentioning

confidence: 99%

Prophylactic administration of a Propionibacterium acnes-killed preparation increases survival in animals with polymicrobial sepsis via the nitric oxide and TNF- pathway

Santana¹,

Aguiar²,

AraÃojo³

et al. 2016

Afr. J. Pharm. Pharmacol.

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Propionibacterium acnes (P. acnes) is a gram-positive anaerobic microorganism present in human skin, and has being widely used in clinical trials as a suitable candidate for therapeutic approach to sepsis. A previous study performed by our research group demonstrated that a P. acne killed preparation had an important immunomodulatory role in severe sepsis. Hence, this study we evaluated the immunomodulatory effect of P. acnes preparation on sub-lethal sepsis using a clinically relevant animal model of polymicrobial sepsis. Cecal ligation and puncture (CLP) was performed in male mice under anesthesia. The group pretreated with the P. acnes-killed preparation showed 80% survival at the end of the experiment (10 days) while the sub-lethal group showed 40% survival. There was an increase in the recruitment of leukocytes to the infection site in animals pretreated with the P. acnes-killed preparation, which was confirmed by a histological analysis of the cecum. Reduction in the Tumor Necrosis Factoralpha (TNF-alpha) level was observed in the group prophylactically treated with the P. acnes-killed preparation compared to the level in the sub-lethal group. However, significant changes were not observed in Interleukin-1β (IL-1) and Interleukin-6 (IL-6) levels between the groups prophylactically treated with P. acnes and those subjected to sub-lethal sepsis. Treatment with the P. acnes-killed preparation also reduced lung injury and reduced the nitric oxide (NO) levels in the peritoneal fluid of the treated animals compared to the levels recorded in the sub-lethal group, a result probably related to the increased recruitment of neutrophils and increased survival. The results obtained suggest that prophylactic treatment P. acnes can mitigate the effects of sepsis, increasing the survival of mice.

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“…It is reported that in addition to inhibiting plasmin, trypsin, chymotrypsin, elastase, and various pancreatic enzymes (Nishiyama et al, 1996), UTI also suppresses activation of inflammatory cells (e.g., neutrophils and leukocytes) and the production of inflammatory mediators such as tumor necrosis factor (TNF)-a, and interleukin (IL)-1β, IL-6, IL-8, and IL-15 (Ito et al, 2005;Fang et al, 2011;Cao et al, 2012;Shen et al, 2012;Wang et al, 2013). Therefore, UTI is suggested to be a potential therapeutic agent for ALI (Ito et al, 2005;Fang et al, 2011;Shen et al, 2012;Wang et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Effect of ulinastatin on HMGB1 expression in rats with acute lung injury induced by sepsis

Wang

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to investigate the influence of ulinastatin (UTI) on high mobility group box 1 (HMGB1), tumor necrosis factor (TNF)-a, and interleukin (IL)-6 expression in acute lung injury (ALI) rats with sepsis caused by cecal ligation and puncture (CLP) surgery, as well as to examine the underlying biological mechanism. Thirty rats were randomly and evenly divided into sham (control), CLP, and CLP + UTI groups. Thirty minutes after the surgery, the rats in the CLP + UTI group received UTI via the caudal vein, while normal saline was administered to rats in the other groups. Blood, lung tissues, and bronchoalveolar lavage fluid (BALF) were collected at different time points (6, 12, 24, and 48 h) after surgery for determination of related indicators. Compared with the CLP group, rats in the CLP + UTI group exhibited higher seven day survival rates, less lung injury, and decreased HMGB1 expression in the lung tissue, serum, and BALF. In addition, the levels of TNF-a and IL-6 at 24 h in the CLP + UTI group were markedly lower than those in the CLP group. These results suggest that 4345 UTI effects on HMGB1 expression in ALI rats ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (2): 4344-4353 (2015) by deregulation, UTI might decrease the lung injury and increase the survival time of ALI rats by downregulating HMGB1 expression as well as by inhibiting TNF-α and IL-6 levels in serum and BALF.

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Protective effect of Ulinastatin against murine models of sepsis: Inhibition of TNF-α and IL-6 and augmentation of IL-10 and IL-13

Cited by 72 publications

References 33 publications

Ulinastatin and Septic Cardiac Dysfunction

Ulinastatin and Septic Cardiac Dysfunction

Prophylactic administration of a Propionibacterium acnes-killed preparation increases survival in animals with polymicrobial sepsis via the nitric oxide and TNF- pathway

Effect of ulinastatin on HMGB1 expression in rats with acute lung injury induced by sepsis

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