pediatric-gastroenterology-digestive-diseases-2018-posters

Volume 8

Journal of Gastrointestinal & Digestive System

ISSN: 2161-069X

Page 51

JOINT EVENT

Pediatric Gastro 2018

Digestive Diseases 2018

October 22-23, 2018

October 22-23, 2018 Berlin, Germany

International Conference on

Digestive and Metabolic Diseases

Pediatric Gastroenterology Hepatology & Nutrition

International Conference on

In vivo

cellular and molecular gastroprotective mechanisms of chrysin: Emphasis on oxidative stress,

inflammation and angiogenesis

Mina Y George

Ain Shams University, Egypt

astric ulceration is one of the major gastrointestinal disorders affecting people worldwide. Despite medical advances,

management of gastric ulcer and its complications remains a challenge facing medicine nowadays. In addition, currently

available medicines exhibit limited efficacy and several side effects. Hence, the potential protective effects of chrysin -naturally

occurring flavonoid- were tested against indomethacin-induced gastric ulcer model in rats. In a preliminary study, chrysin

was administered to spargue-Dawly rats (200-220 g) at three different doses; 25, 50 and 100 mg/kg, single oral dose (S.O.D)

compared to omeprazole given at a dose of 30 mg/kg, S.O.D. Indomethacin was administered at a dose of 48 mg/kg, S.O.D.

Chrysin in both doses; 50 and 100mg/kg were effective in promotingmucus secretion and preventing the rise in ulcer and lesion

indices, acid production and histologic changes induced by indomethacin. During investigation of the possible underlying

mechanisms, chrysin pretreatment significantly attenuated indomethacin-induced oxidative injury proved by its effects on

catalase, reduced glutathione and lipid peroxidation levels. In addition, chrysin reduced inflammatory response caused by

indomethacin owing to its effects on nuclear factor-kappa B (NF-κB), tumor necrosis factor-α (TNF-α) and interleukin-1β

(IL-1β). Moreover, chrysin activated peroxisome proliferator activated receptor-ɣ (PPAR-

) leading to a phenotypic switch

from pro-inflammatory M1 macrophages to the anti-inflammatory M2 macrophages evidenced by the upregulated mRNA

expression levels of PPAR-

and M2 marker genes (Arg-1 and CD206) and downregulation of M1 marker genes (IL-6 and

CCL3). Furthermore, chrysin initiated angiogenesis via increasing expression of vascular endothelial growth factor (VEGF),

basic fibroblast growth factor (bFGF) and cluster of differentiation-31 (CD31) resulting in tissue repair. Collectively, these

findings indicate that chrysin possesses a potential protective effect against indomethacin-induced gastric ulcer via suppressing

oxidative stress, inflammation and initiating angiogenesis.

J Gastrointest Dig Syst 2018, Volume 8

DOI: 10.4172/2161-069X-C7-083