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Styli cum stigmatis Zeae maydis
min/100 g bw; p < 0.05) and the Na + filtered load (41.9–34.3, p < 0.05) decreased,
and creatinine and Li clearances and Na + excretion were unchanged,
while K + excretion (0.10–0.22 µEq/min/100 g bw; p < 0.001) increased.
Thus, at a water-loading of 2.5 ml/100 g bw, the extract increased diuresis at
a dose of 500 mg/kg, and increased excretion of K + at doses of 350 and
500 mg/kg. At a water-loading of 5 ml/100 g bw, excretion of K + increased at
a dose of 500 mg/kg, but glomerular filtration decreased (64).
Prevention of diabetic complications
The aldehyde group of reducing sugar and amino residues in protein react
and result in the formation of aggregates (advanced glycation end-products)
such as N-ε-(carboxymethyl) lysine. Formation of these aggregates in the
human body through glycation is associated with the induction of diabetic
complications. Accumulation of N-ε-(carboxymethyl) lysine in the kidneys
of subjects with diabetes has been reported. The inhibition of N-ε-
(carboxymethyl) lysine accumulation by the flavone C-glucoside, chrysoeriol
6-C-β-fucopyranoside, isolated from the style of Zea mays, was calculated
to be 80.7% (46). The same glycation inhibiting action was later shown for
the corresponding 6-boivinoside. Similar derivatives of chrysoeriol, but with
one more sugar attached, were inactive. Of the purines and pyrimidines present
in Zea mays, only guanosine was found to be a glycation inhibitor (65).
The efficacy of a water extract of styles of Zea mays on diabetic nephropathy
evoked by intravenous injection of streptozocin (40 mg/kg) was
investigated in rats randomly allocated either to a control group (non-diabetic
rats, n = 5), a non-treated group of diabetic rats (n = 9), or a group of
treated diabetic rats (n = 8). The treated groups were given tap water containing
an extract of dry styles at a concentration of 0.15% (w/v) (about
0.2 g/day), while the animals in the control and non-treated groups were
given ordinary tap water. The rats were allowed free access to their water
for 12 weeks. At 12 weeks, urine was collected for 24 hours using a metabolic
cage, followed by the collection of a blood sample and a kidney sample
after killing the animals. Plasma glucose, haemoglobin, fructosamine,
creatinine, urinary creatinine, urinary albumin excretion and other clinical
parameters were also measured. Creatinine clearance was calculated per
100 g of body weight. The difference in body weight observed between the
non-treated diabetic rats and the control rats was significant (p < 0.01). The
plasma glucose levels in the non-treated diabetic rats were significantly
higher than in the control animals (p < 0.01); however, there was no difference
in the plasma glucose, fructosamine or haemoglobin levels between
treated diabetic rats and non-treated diabetic rats. The ratios of kidney
weight to body weight were significantly higher in non-treated diabetic rats
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