Alpha-Melanocyte Stimulating Hormone Protects Pancreatic Islet Dysfunction by Peripheral Blood Mononuclear Cells in vitro.
- Author:
Eun Jung JUNG
1
;
Duck Jong HAN
;
Sung Ho CHANG
;
Dong Gyun LIM
;
Yu Mee WEE
;
Jin Hee KIM
;
Yang Hee KIM
;
Sung Kyung KOO
;
Monica CHOI
;
Kwan Tae PARK
;
Song Cheol KIM
Author Information
1. Department of Surgery, Ulsan University College of Medicine & Asan Medical Center, Korea. drksc@amc.seoul.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Alpha-melanocyte-stimulating hormone;
Pancreatic islet;
Blood mononuclear cell;
Anti-inflammatory reaction
- MeSH:
alpha-MSH;
Animals;
Apoptosis;
Cell Death;
Coculture Techniques;
Cytokines;
Graft Survival;
Insulin;
Ionomycin;
Islets of Langerhans Transplantation;
Islets of Langerhans*;
Nitric Oxide;
Rats;
Tumor Necrosis Factor-alpha
- From:The Journal of the Korean Society for Transplantation
2006;20(1):41-48
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: The alpha-melanocyte-stimulating hormone (alpha-MSH) has been shown to interact with various cells of the immune and inflammatory system and down-regulate either the production or the action of the pro-inflammatory cytokines. In this study, we investigated the potential of alpha-MSH on preventing pancreatic islet cell from death and dysfunction by inflammatory cytokines released from peripheral blood mononuclear cells (PBMCs) in rat. METHODS: Rat pancreatic islets were co-cultured with PBMCs, stimulated by phorbol myrstic acid and ionomycin. alpha-MSH was treated to PBMCs for 2 hours before co-culture. Viability and apoptosis of islets were observed by MTT and FACS. Inflammatory cytokines and nitric oxide (NO) were measured. Insulin release from islet co-cultured with mononuclear cells was checked for the islet function. RESULTS: In comparison to control group, viability of islets with alpha-MSH treated mononuclear cells was increased and apoptosis was reduced significantly. Inflammatory cytokines such as TNF-alpha and IL-1beta were reduced in alpha-MSH-treated group. NO production in alpha-MSH-treated group was decreased. Insulin secretory function of islet was recovered in condition of alpha-MSH treatment. CONCLUSION: This study demonstrates that alpha-MSH protects cell death and preserves the secretory function of pancreatic islet cells from the pro-inflammatory reaction of mononuclear cells, and may have the potential to improve the graft survival in clinical islet transplantation.
