title: Histological and immunohistochemical effects of L-arginine and silymarin on TNBS-induced inflammatory bowel disease in rats.
abstract: Inflammatory bowel disease (IBD) is a chronic disease that affects quality of life. Various mediators are involved in IBD pathogenesis including inducible nitric oxide synthase (iNOS), nuclear factor kappa B (NF-κB), cytochrome c, heat shock protein 70 (HSP70) and tumor necrosis factor (TNF)-α. L-Arginine (L-Arg) can be depleted in IBD, and silymarin inhibits neutrophil infiltration, NF-κB, and TNF-α, which have crucial roles in inducing IBD. This study aimed to investigate whether silymarin and L-Arg supplementation decreases IBD progression in trinitrobenzine-sulfonic acid (TNBS)-induced colitis. Fifty adult male albino rats were randomized into five groups (10 animals per group): Group I rats orally received 100 mg silymarin/kg body weight once daily; Group II rats orally received 2 mg L-Arg/100 g body weight in 5 mL distilled water once daily; Group III rats rectally received 0.85 mL TNBS in 50% ethanol to induce colitis; Group IV rats were treated similar to group III and, on recovery from anesthesia, received silymarin as described for group I; and Group V rats were treated similar to group III and, on recovery from anesthesia, received L-Arg as described for group II. On day 7, the rats were anesthetized, and blood samples were collected to determine the serum concentrations of TNF-α. Laparotomy and total colectomy were performed for macroscopic, histological, and immunohistochemical investigations. The results showed that silymarin and L-Arg macroscopically and microscopically ameliorated TNBS-induced colitis; significantly decreased the serum levels of TNF-α; inhibited the colonic expression of iNOS, NF-κB, and cytochrome c; and increased expression of HSP70. Our results suggest that these complementary medicines could be used to supplement current treatments for IBD.
authors.affiliation: Department of Physiology, Prince Sultan Ben Abdulaziz College of EMS and Department of Medical Education, College of Medicine, King Saud University, Riyadh, KSA.
authors.forename: Abdul
authors.initials: A
authors.lastname: Al-Drees
authors.affiliation: College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia and Department of Histology, Faculty of Medicine, Suez Canal University, Ismailia, Egypt. msalah28@hotmail.com.
authors.forename: Mahmoud Salah
authors.initials: MS
authors.lastname: Khalil
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001120:Arginine / Q000494:pharmacology*; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D015212:Inflammatory Bowel Diseases / Q000139:chemically induced / Q000473:pathology*; D008297:Male; D011897:Random Allocation; D051381:Rats; D012838:Silymarin / Q000494:pharmacology*; D014302:Trinitrobenzenesulfonic Acid / Q000633:toxicity
chemical_list: D000975:Antioxidants; D012838:Silymarin; D014302:Trinitrobenzenesulfonic Acid; D001120:Arginine