Background:
Diabetes mellitus is a metabolic disorder associated with relative or
absolute insulin deficiency or resistance, characterized by hyperglycemia.
Modern prescriptions such as pioglitazone have better therapeutic potential,
but its side effects and financial burden for developing countries have
motivated the researchers to find alternative natural drugs to compete
hyperglycemia in patients with diabetes. The present study was conducted to
explore the therapeutic potential of selected medicinal plants for the
treatment of diabetes as an alternative to allopathic medicines.
Method:
In present study, hydroalcoholic extracts of
Curcuma longa
,
Lavandula stoechas
,
Aegle marmelos,
and
Glycyrrhiza glabra
and their polyherbal preparation
(PHP) as compound drug were investigated for their antihyperglycemic
potential in alloxan-induced diabetic mice. The study subjects (mice) were
divided into different groups as normal control, diabetic control,
pioglitazone treated (standard drug), test groups (plant extract treated 50,
100, and 150 mg/kg body weight), and PHP-treated group. Blood glucose
concentration of all the study animals was determined by Glucose strip test.
Qualitative phytochemical analysis of all the plant extracts was also
performed following standard methods.
Result:
It was investigated that treatment of alloxan-induced diabetic mice with
hydroalcoholic extracts of studied medicinal plants showed significant
(
P
< .05) effects on fasting blood glucose levels
(from baseline to normal range) in a manner comparable to that of the
reference drug, pioglitazone (1 mg/kg body weight intraperitoneal). The
tested plant extracts significantly (
P
< .05) reduced
the glucose concentration in blood of diabetes-induced mice in a
dose-dependent manner.
Conclusion:
It could be concluded that studied medicinal plants have antihyperglycemic
activity. The study findings favor the use of traditional herbal medicinal
practices for the management of diabetes that might due to the presence of
bioactive phytoconstituents in plants. However, larger studies are required
to identify, isolate, and characterize the bioactive phytoconstituents
responsible for antihyperglycemic activity of studied medicinal plants.
Previous studies have shown that hypoxia induces nitric oxide synthase-mediated generation of nitric oxide free radicals leading to peroxynitrite production. The present study tests the hypothesis that hypoxia results in NO-mediated modification of Na+, K+-ATPase in the fetal brain. Studies were conducted in guinea pig fetuses of 58-days gestation. The mothers were exposed to FiO2 of 0.07% for 1 hour. Brain tissue hypoxia in the fetus was confirmed biochemically by decreased ATP and phosphocreatine levels. P2 membrane fractions were prepared from normoxic and hypoxic fetuses and divided into untreated and treated groups. The membranes were treated with 0.5 mM peroxynitrite at pH 7.6. The Na+, K+-ATPase activity was determined at 37 degrees C for five minutes in a medium containing 100 mM NaCl, 20 mM KCl, 6.0 mM MgCl2, 50 mM Tris HCl buffer pH 7.4, 3.0 mM ATP with or without 10 mM ouabain. Ouabain sensitive activity was referred to as Na+, K+-ATPase activity. Following peroxynitrite exposure, the activity of Na+, K+-ATPase in guinea pig brain was reduced by 36% in normoxic membranes and further 29% in hypoxic membranes. Enzyme kinetics was determined at varying concentrations of ATP (0.5 mM-2.0 mM). The results indicate that peroxynitrite treatment alters the affinity of the active site of Na+, K+-ATPase for ATP and decreases the Vmax by 35% in hypoxic membranes. When compared to untreated normoxic membranes Vmax decreases by 35.6% in treated normoxic membranes and further to 52% in treated hypoxic membranes. The data show that peroxynitrite treatment induces modification of Na+, K+-ATPase. The results demonstrate that peroxynitrite decreased activity of Na+, K+-ATPase enzyme by altering the active sites as well as the microenvironment of the enzyme. We propose that nitric oxide synthase-mediated formation of peroxynitrite during hypoxia is a potential mechanism of hypoxia-induced decrease in Na+, K+-ATPase activity.
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