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Effect
of polyunsaturated fatty acids on dexamethasone-induced gastric mucosal damage
Manjari
V, Das UN
Department
Of Internal Medicine, Clinical Immunology and Biochemistry, L. V. Prasad Eye
Institute, Hyderabad, India
Background.
Increased dietary intake of polyunsaturated fatty acids (PUFAs) is known to be
associated with a decrease in the incidence of peptic ulcer disease possibly due
to increase in the synthesis of prostaglandins.
But, it is also likely that conversion of PUFAs to PGs may not always be
required for gastric mucosal protection.
Present study was designed to study the role of PUFAs in pathobiology of steroid
induce gastric damage in rats.
Methods.
Wistar rats were treated with 5 mg/kg bodyweight of dexamethasone to induce
gastric mucosal ulcers.
Effects of PUFAs was studied by supplementation of Fish oil (rich in n-3 EPA and
DHA) and AA rich oil.
Famotidine was used as a positive control.
Generation of lipid peroxides, nitric oxide and the activity of anti-oxidant
enzymes were also studied.
Results.
Dexamethasone induced ulceration was associated with changes in the phospholipid
fatty acid profile, levels of lipid peroxidation products, nitric oxide and
activity of anti-oxidant enzymes.
The fatty acid profile showed an increase in LA and a decrease in other PUFAs
like GLA, AA, EPA and DHA.
When PUFAs were supplemented in the form of Fish oil and AA rich oil or when the
animals were treated with H2-blocker, famotidine, there was a decrease in the
incidence of ulceration in the animals associated with near normalization of
changes in the phospholipid fatty acid profile.
The levels of lipid peroxides, nitric oxide, and anti-oxidant activity also
reverted to control values.
Conclusions.
Dexamethasone induced gastric ulceration was prevented by PUFAs.
This is supported by the results of our earlier study where in it was noted that
in patients with DU plasma lipid peroxides, nitric oxide and phospholipid fatty
acid pattern and red cell antioxidant activity were altered similar to those
seen in dexamethasone treated group of the present study.
These abnormalities, similar to the PUFA treated groups of the present study,
reverted to normalcy following treatment of the patients with lansoprazole, a
proton pump inhibitor.
Further, PUFAs are known to inhibit the growth of Helicobacter pylori in vitro.
Hence, it is concluded that PUFAs, free radicals, nitric oxide and anti-oxidants
play a significant role in the pathobiology of peptic ulcer.
PMID:
10780873 [PubMed - indexed for MEDLINE]
Source:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10780873&dopt=Abstract
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