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.
Highlights
Colorectal cancer has become prevalent in Western societies, and in other parts of the world (Torre et al, 2015)
Colorectal Inhibitory effects of Perilla frutescens extract (PE) against dextran sulfate sodium (DSS)-induced inflammatory tissues from DSS-treated mice showed collapse and expansion events in mouse colon were verified by histological, of epithelium which were accompanied by infiltration of inflammatory cells (Figure 2B) and overexpression of COX-2, inducible nitric oxide synthase (iNOS), and cyclin D1 (Figures 3A,B)
PE protected the epithelium from DSS-induced colitis as evidenced by attenuation of morphological and biochemical alterations related to inflammatory colonic tissue damage
Summary
Colorectal cancer has become prevalent in Western societies, and in other parts of the world (Torre et al, 2015). Patients with inflammatory bowel disease (IBD), such as ulcerative colitis and Crohn’s disease, have been at increased risk for developing colorectal cancer (Kim and Chang, 2014). IBD is an illness in which colon becomes inflamed and caused by genetic problems, Perilla frutescens Inhibits Experimental Colitis immune disorders, environmental conditions, and infections (Ananthakrishnan, 2015). Multiple mechanisms, including overproduction of reactive oxygen species (ROS) in the inflamed colonic mucosa, immune response by mucosal inflammatory mediators, and altered intestinal microbiota, are speculated to be involved the pathogenesis of IBD. Elevated expression and/or activity of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) have been associated with IBD and inflammation-associated carcinogenesis. INOS is responsible for production of nitric oxide (NO) derived from L-arginine. Excessive formation of NO causes nitrosative stress which leads to cell cycle disorders, apoptotic cell death, and DNA damage (Aktan, 2004)
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