Horm Metab Res 2017; 49(09): 693-700
DOI: 10.1055/s-0043-112761
Endocrine Research
© Georg Thieme Verlag KG Stuttgart · New York

11-Keto-β-Boswellic Acid Inhibits Lymphocyte (CD3) Infiltration Into Pancreatic Islets of Young None Obese Diabetic (NOD) Mice

Ahmed M. Shehata
1   Department of Pharmacology, Institute of Pharmaceutical Sciences, University of Tübingen, Tübingen, Germany
2   Department of Pharmacology, Faculty of Pharmacy, Beni-Suef University, Beni Suef, Egypt
,
Leticia Quintanilla-Fend
3   Institute of Pathology and Neuropathology, University of Tübingen and Comprehensive Cancer Center, University Hospital Tübingen, Tübingen, Germany
,
Sabrina Bettio
3   Institute of Pathology and Neuropathology, University of Tübingen and Comprehensive Cancer Center, University Hospital Tübingen, Tübingen, Germany
,
Zahra Kamyabi-Moghaddam
3   Institute of Pathology and Neuropathology, University of Tübingen and Comprehensive Cancer Center, University Hospital Tübingen, Tübingen, Germany
,
Ursula A. Kohlhofer
3   Institute of Pathology and Neuropathology, University of Tübingen and Comprehensive Cancer Center, University Hospital Tübingen, Tübingen, Germany
,
Werner A. Scherbaum
4   Heinrich-Heine-University, University Hospital Düsseldorf, Düsseldorf, Germany
,
Hermann P.T. Ammon
1   Department of Pharmacology, Institute of Pharmaceutical Sciences, University of Tübingen, Tübingen, Germany
› Author Affiliations
Further Information

Publication History

received 08 September 2016

accepted 30 May 2017

Publication Date:
31 July 2017 (online)

Abstract

11-Keto-β-Boswellic acid (KBA) has been shown to prevent infiltration of lymphocytes into pancreatic islets and appearance of peri-insular apoptotic cells in an animal model of autoimmune diabetes caused by injection of Multiple Low Doses of Streptozotocin (MLD-STZ), which is a chemical compound belonging to the class of nitrososureas. The aim of this work was to study whether or not KBA can also prevent/attenuate infiltration of lymphocytes into pancreatic islets and appearance of peri-insular apoptotic cells in an animal model of autoimmune diabetes caused by genetic dysfunction resembling human type 1 diabetes in several important features. Four weeks old female NOD mice received daily i.p. injections of 7.5 mg/kg of KBA over a period of 3 weeks. Compared to 4 weeks old animals there was significant infiltration of lymphocytes (CD3) into pancreatic islets and appearance of peri-insular apoptotic cells in the period between 4 and 7 weeks. During this time plasma glucose dropped significantly and body weight did not increase. As far as pro-inflammatory cytokines are concerned, except a small increase of IFN-γ, there was no change in the blood. In mice that had been treated with KBA between 4 and 7 weeks after birth no significant infiltration of lymphocytes into pancreatic islets and appearance of peri-insular apoptotic cells was observed, when compared to 4 weeks old mice. Moreover, there was no drop of blood glucose and the animals gained body weight. It is concluded that – similar to the model of MLD-STZ-diabetes – also in the NOD mouse model KBA is able to attenuate or even prevent development of insulitis, suggesting that KBA protects islets from autoimmune reaction regardless whether the signal is provided by a chemical compound or by genetic dysfunction. Whether this also holds for human type 1 diabetes remains to be established.

 
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