Protective efficacy of ursodeoxycholic acid nanoparticles in animal model of inflammatory bowel disease

De, Amitabha; Sana, Santanu; Datta, Sriparna; Mukherjee, Arup

doi:10.3109/02652048.2014.918666

Cited by 12 publications

(5 citation statements)

References 46 publications

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“…13,115,116 Several formulations of UDCA have been developed to try to increase colonic delivery, including conjugation with glutamate, nanosuspensions/nanoparticles, and microbial derivation. [116][117][118] The UDCA-glutamate prevents absorption and biotransformation in the small intestine but takes advantage of the peptide bond cleavage within the colonic brush boarder enzymes to remove the glutamate thus allowing for colonic delivery of UDCA. 116 UDCA nanosuspensions encapsulate this bile acid and allow for increased colonic transit time.…”

Section: Ursodeoxycholic Acid Modulation Of Microbiota-bile Acid-hostmentioning

confidence: 99%

“…116 UDCA nanosuspensions encapsulate this bile acid and allow for increased colonic transit time. 117,118 UDCA could also be microbially derived from administration of UDCA-producing bacteria, such as Clostridium baratii or Ruminococcus gnavus N53 (Figure 3). 61,90 Additional research is required to investigate the use of UDCA-producing bacteria in vivo.…”

Section: Ursodeoxycholic Acid Modulation Of Microbiota-bile Acid-hostmentioning

confidence: 99%

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Diversification of host bile acids by members of the gut microbiota

2019

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Bile acid biotransformation is a collaborative effort by the host and the gut microbiome. Host hepatocytes synthesize primary bile acids from cholesterol. Once these host-derived primary bile acids enter the gastrointestinal tract, the gut microbiota chemically modify them into secondary bile acids. Interest into the gut-bile acid-host axis is expanding in diverse fields including gastroenterology, endocrinology, oncology, and infectious disease. This review aims to 1) describe the physiologic aspects of collaborative bile acid metabolism by the host and gut microbiota; 2) to evaluate how gut microbes influence bile acid pools, and in turn how bile acid pools modulate the gut microbial community structure; 3) to compare species differences in bile acid pools; and lastly, 4) discuss the effects of ursodeoxycholic acid (UDCA) administration, a common therapeutic bile acid, on the gut microbiota-bile acid-host axis.

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Section: Ursodeoxycholic Acid Modulation Of Microbiota-bile Acid-hostmentioning

confidence: 99%

Section: Ursodeoxycholic Acid Modulation Of Microbiota-bile Acid-hostmentioning

confidence: 99%

Diversification of host bile acids by members of the gut microbiota

2019

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“…The biological actions of UDCA have been mostly studied in the liver, where it has been shown to have immunomodulatory and anti-apoptotic effects, and to prevent cytokine release from hepatocytes (1,34,36). Interestingly, several studies have shown that UDCA also exerts protective actions in animal models of intestinal inflammation, effects which were associated with reduced levels of mucosal cytokines, nitric oxide, and prevention of epithelial apoptosis (8,22,23,28).…”

Section: Il-8 Pg/mlmentioning

confidence: 99%

Ursodeoxycholic acid inhibits TNFα-induced IL-8 release from monocytes

O’Dwyer

Lajczak

Keyes

et al. 2016

American Journal of Physiology-Gastrointestinal and Liver Physi

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Monocytes are critical to the pathogenesis of inflammatory bowel disease (IBD) as they infiltrate the mucosa and release cytokines that drive the inflammatory response. Ursodeoxycholic acid (UDCA), a naturally occurring bile acid with anti-inflammatory actions, has been proposed as a potential new therapy for IBD. However, its effects on monocyte function are not yet known. Primary monocytes from healthy volunteers or cultured U937 monocytes were treated with either the proinflammatory cytokine, TNFα (5 ng/ml) or the bacterial endotoxin, lipopolysaccharide (LPS; 1 μg/ml) for 24 h, in the absence or presence of UDCA (25-100 μM). IL-8 release into the supernatant was measured by ELISA. mRNA levels were quantified by qPCR and changes in cell signaling proteins were determined by Western blotting. Toxicity was assessed by measuring lactate dehydrogenase (LDH) release. UDCA treatment significantly attenuated TNFα-, but not LPS-driven, release of IL-8 from both primary and cultured monocytes. UDCA inhibition of TNFα-driven responses was associated with reduced IL-8 mRNA expression. Both TNFα and LPS stimulated NFκB activation in monocytes, while IL-8 release in response to both cytokines was attenuated by an NFκB inhibitor, BMS-345541. Interestingly, UDCA inhibited TNFα-, but not LPS-stimulated, NFκB activation. Finally, TNFα, but not LPS, induced phosphorylation of TNF receptor associated factor (TRAF2), while UDCA cotreatment attenuated this response. We conclude that UDCA specifically inhibits TNFα-induced IL-8 release from monocytes by inhibiting TRAF2 activation. Since such actions would serve to dampen mucosal immune responses in vivo, our data support the therapeutic potential of UDCA for IBD.

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“…Проводится экспериментальное исследование на животных моделях УДХК в виде поликатионных наночастиц (UNPs), что возможно сможет повысить эффективность препарата. Так же продолжается активное изучение профилактическое применение новых производных УДХК, например нор-УДХК, таурохолевой кислоты [21][22][23].…”

Section: клинико-патогенетическое обоснование «гепатопротекции сопровunclassified

Ursodeoxycholic acid: paradigmatic transformation of the prevention of drug-induced liver lesions in clinical practice

2017

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In the article argued the necessity of using tactics "hepatoprotektor's escort" in clinical practice. In it demonstrates data about new effects of Ursodeoxycholic Acid and the capabilities of its application as a universal hepatoprotector have been elucidated. Inclusion of Ursodeoxycholic Acid in the combined therapy enhances the effectiveness of treatment of patients in many branches of medicine.Keywords: Ursodeoxycholic Acid -drug-induced liver lesions. РЕЗюМЕ В статье аргументирована необходимость использования клинической практике тактики «гепатопротекции сопровождения». Приве-дены данные о новых эффектах урсодезоксихолевой кислоты. Освещены возможности ее использования как универсального гепатопро-тектора. Включение урсодезоксихолевой кислоты в комплексную терапию способствует повышению эффективности лечения пациентов во многих отраслях медицины.Ключевые слова: урсодзоксихолевая кислота; лекарственно-индуцированные поражения печени.

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Protective efficacy of ursodeoxycholic acid nanoparticles in animal model of inflammatory bowel disease

Abstract: This study presents the improved efficacy of UNPs in animal model of IBD due to complete release of drug at the desired site of action.

Cited by 12 publications

References 46 publications

Diversification of host bile acids by members of the gut microbiota

Diversification of host bile acids by members of the gut microbiota

Ursodeoxycholic acid inhibits TNFα-induced IL-8 release from monocytes

Ursodeoxycholic acid: paradigmatic transformation of the prevention of drug-induced liver lesions in clinical practice

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