Boswellia and diabetes prevention.
Boswellia (Health aspects)
|Publication:||Name: Australian Journal of Medical Herbalism Publisher: National Herbalists Association of Australia Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2011 National Herbalists Association of Australia ISSN: 1033-8330|
|Issue:||Date: Winter, 2011 Source Volume: 23 Source Issue: 4|
Shehata A, Quintanilla-Fend L, Bettio S, Singh C, Ammon H. 2011.
Prevention of multiple low-dose streptozotocin (MLD-STZ) diabetes in
mice by an extract from gum resin of Boswellia serrata (BE). Phytomed
Type 1 diabetes mellitus is an autoimmune disease in which immune driven inflammatory processes cause pancreatic [beta] cell destruction and an insufficient or complete lack of insulin production. This and other autoimmune diseases, are marked by overproduction of inflammatory cytokines such as NFKB, TNF-[alpha], IFN-Y, IL-1B and IL-2. In type 1 diabetes much of this inflammatory and cell destruction occurs as a silent process, only becoming manifest once a large number of P cells have been destroyed.
As Boswellia serrata (boswellia) has been shown in a number of studies to possess anti-inflammatory activity, the researchers here set out to see if it could modulate the development of type 1 diabetes and prevent hyperglycemia, inflammation of pancreatic islets and increase of proinflammatory cytokines in a murine model.
A condition very similar to type 1 diabetes can be induced in animals by the administration of multiple low doses of streptozotocin (STZ). In this study, 5 days of treatment produced permanent increase of blood glucose, infiltration of lymphocytes into pancreatic islets, apoptosis of peri-insular cells after 10 days as well as shrinking of islet tissue after 35 days. There was also an increase of granulocyte colony stimulating factor (G-CSF), granulocyte/macrophage colony stimulating factor (GM-CSF) and proinflammatory cytokines (IL1A, IL-1B, IL-2, IL-6, IFN-Y, TNF-a) in the blood.
These STZ treated mice, as well as control mice, were then given boswellia 150 mg/kg intraperitoneally once daily for 5 or 10 days. The boswellia used was an ethanolic extract containing 5.48% KBA and 4.66% AKBA (two different types of active boswellic acid). A second control group received only solvent in their ten days of injections.
Blood samples were taken from the animals at baseline and 5, 10, 14, 21, 28 and 35 days after the beginning of the experiment. Some histological samples were also collected at days 10 and 35.
After 5 days of STZ treatment there was no change in blood glucose, however starting after 10 days there was a continuous increase over a period of 35 days. When boswellia was given to the STZ-treated rats for 5 days there was no effect on blood glucose levels. Upon cessation of boswellia there was a continuous rise in blood glucose as with those animals not taking the herb. However in those animals that received the extract for ten days there was no subsequent rise in blood glucose, even post treatment.
Mice who had received STZ treatment had drastically shrunken pancreatic islets, however those who had simultaneously received boswellia had normal looking islets. The ten days of herbal treatment also prevented elevation of G-CSF and significantly reduced increase of GM-CSF in the serum as well as significantly diminishing the amounts of pro-inflammatory cytokines in the serum.
The data from this animal model suggests that the development of hyperglycemia and insulitis in type 1 diabetes may be prevented through administration of an ethanolic extract of Boswellia serrata. The mechanism is likely to be related to boswellia's anti-inflammatory action. Only further clinical studies can provide proof.
Tessa Finney-Brown MNHAA
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