Perilla frutescens Extracts Protects against Dextran Sulfate Sodium-Induced Murine Colitis: NF-κB, STAT3, and Nrf2 as Putative Targets

Abstract

Perilla frutescens is a culinary and medicinal herb which has a strong anti-inflammatory and antioxidative effects. In the present study, we investigated the effects of Perilla frutescens extract (PE) against dextran sulfate sodium (DSS)-induced mouse colitis, an animal model that mimics human inflammatory bowel disease (IBD). Five-week-old male ICR mice were treated with a daily dose of PE (20 or 100 mg/kg, p.o.) for 1 week, followed by administration of 3% DSS in double distilled drinking water and PE by gavage for another week. DSS-induced colitis was characterized by body weight loss, colon length shortening, diarrhea and bloody stool, and these symptoms were significantly ameliorated by PE treatment. PE administration suppressed DSS-induced expression of proinflammatory enzymes, including cyclooxygenase-2 and inducible nitric oxide synthase as well as cyclin D1 , in a dose-dependent fashion. Nuclear factor-kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3) are major transcriptional regulators of inflammatory signaling. PE administration significantly inhibited the activation of both NF-κB and STAT3 induced by DSS, while it elevated the accumulation of Nrf2 and heme oxygenase-1 in the colon. In another experiment, treatment of CCD841CoN human normal colon epithelial cells with PE (10 mg/ml) resulted in the attenuation of the tumor necrosis factor-α-induced expression/activation of mediators of proinflammatory signaling. The above results indicate that PE has a preventive potential for use in the management of IBD.

Protective Effect of Cicer arietinum L. (Chickpea) Ethanol Extract in the Dextran Sulfate Sodium-Induced Mouse Model of Ulcerative Colitis

“…The functional interactions between NF-κB and STAT3 enhance inflammation in the intestinal mucosa and have been investigated in other studies [25,26]. In contrast, abrogation of NF-κB and STAT3 activation has been reported to be associated with improvements in intestinal homeostasis in DSS-administrated mice [27]. The present study showed that CEE administration potently attenuated the DSS-mediated increases in the phosphorylation levels of p65 and STAT3 in colonic tissues.…”

Periplaneta americana Ameliorates Dextran Sulfate Sodium-Induced Ulcerative Colitis in Rats by Keap1/Nrf-2 Activation, Intestinal Barrier Function, and Gut Microbiota Regulation

“…At present, an increasing number of researches ( Yang et al, 2016 ; Ahmed et al, 2017 ) have begun to focus on the role of Nrf2/Keap1 pathway in the inflammation-associated pathogenesis, as well as the suppression of pro-inflammatory signaling pathways. Besides, previous studies have demonstrated the decreased expression of Nrf2 in dextran sulfate sodium (DSS)-induced UC model and the important role of Nrf2 signaling pathway in UC treatment by some chemo-preventive agents ( Dae Park et al, 2017 ; Seo et al, 2017 ; Liu et al, 2018 ; Tan and Zheng, 2018 ).…”

Exclusive enteral nutrition protects against inflammatory bowel disease by inhibiting NF‑κB activation through regulation of the p38/MSK1 pathway

“…The DSS-induced colitis model mimics human inflammatory bowel disease appropriately ( 42 ); therefore, this model was used to investigate the effect of EEN on colitis. In the present study, EEN attenuated colitis injury and inflammatory symptoms induced by DSS, such as weight loss, shortening of colon length and colonic tissue damage.…”