Beneficial effect of Flos magnoliae extract on multiple low dose streptozotocin-induced type 1 diabetes development and cytokine-induced β-cell damage

• Published in: International journal of molecular medicine 2008-10, Vol.22 (4), p.481-488
• Main Authors: Kim, Eun-Kyung, Song, Mi-Young, Kim, In-Seob, Moon, Woo, Ryu, Do-Gon, So, Hong-Seob, Park, Raekil, Park, Jin-Woo, Kwon, Kang-Beom, Park, Byung-Hyun
• Format: Article
• Language: English
• Subjects: Animals; Cell Death - drug effects; Cell Line; Cytokines - pharmacology; Diabetes Mellitus, Experimental - drug therapy; Diabetes Mellitus, Experimental - pathology; Diabetes Mellitus, Type 1 - drug therapy; Diabetes Mellitus, Type 1 - pathology; DNA - metabolism; Female; Glucose - pharmacology; Insulin - metabolism; Insulin Secretion; Insulin-Secreting Cells - drug effects; Insulin-Secreting Cells - enzymology; Insulin-Secreting Cells - pathology; Magnolia - chemistry; Male; Mice; Mice, Inbred ICR; NF-kappa B - metabolism; Nitric Oxide - biosynthesis; Nitric Oxide Synthase Type II - genetics; Nitric Oxide Synthase Type II - metabolism; Phytotherapy; Plant Extracts - therapeutic use; Protein Binding - drug effects; Rats; Rats, Sprague-Dawley; Streptozocin - administration & dosage
• ISSN: 1107-3756
• DOI: 10.3892/ijmm_00000046

In the present study, Flos magnoliae extract (FME) was evaluated to determine if it could protect pancreatic β-cells against multiple low dose streptozotocin (MLDS) and interleukin-1β and interferon-γ. Injection of mice with MLDS resulted in hyperglycemia and hypoinsulinemia, which was confirmed by immunohistochemical staining. However, the induction of diabetes by MLDS was completely prevented when mice were pretreated with FME. FME also effectively protected β-cells against cytokine toxicity, which was demonstrated by an increase in the viability of rat insulinoma RINm5F cells and by preserved insulin secreting responses to glucose in isolated rat islets. Moreover, cytokine-induced nitric oxide production and iNOS mRNA and protein expression were significantly reduced in RINm5F cells and islets that were preincubated with FME. The molecular mechanism by which FME inhibits iNOS gene expression in in vitro and in vivo appears to involve inhibition of NF-κB activation. Taken together, these results reveal the possible therapeutic value of FME for the prevention of type 1 diabetes progression.