Summary: | 碩士 === 國立臺灣大學 === 食品科技研究所 === 85 === Oxidative modification of low density lipoprotein (LDL)
plays a key role in the pathogenesis of
atherosclerosis. Antioxidants, which can effectively inhibit
LDL oxidation, may reduce early
atherogenesis and slow down the progression to advanced stage.
Oxidized LDL (oxLDL), which is no
longer recognized by LDL receptor, is formed in the intimal
area and taken up by the scavenger
receptors of monocyte-derived macrophages, a process resulting
in the formation of foam cells.
Previous studies have reported that tea has a beneficial effect
in lowering plasma cholesterol
and preventing coronary heart disease. As potent antioxidants,
catechins are suspected to exhibit
the preventive effect in tea. This thesis intends to elucidate
the potential of Pu-Erh-Tou tea,
a fermented tea, to prevent LDL from oxidative modification in
vitro and ex vivo. DPPH radical
scavenging and inhibition of Cu2+-induced human LDL oxidation
were chosen as the two in vitro
assay systems. Male Sprague Dawley rats fed with a 1.0%
cholesterol diet were used as the animal
model.
Results showed that the aqueous extracts of Pu-Erh-Tou
(PET), green, pao-chung, oolong teas
(IC50 values were 8.3, 7.5, 8.0 and 8.2 mg/mL, respectively)
scavenged DPPH free radical better
than that of black tea (14.3 mg/mL). The antioxidant potentials
(IC50 values) to inhibit Cu2+-
induced LDL oxidation were PET (1.4 mg/mL), green tea (1.8 mg/
mL), pao-chung tea (2.1 mg/mL),
oolong tea (2.5 mg/mL), and black tea (3.3 mg/mL). Evidently,
PET contained strong antioxidants
that were capable of inhibiting human LDL oxidation in vitro.
Male Sprague Dawley rats (body
weight 216+20 g) were randomly assigned into four groups.
Animals in each group were fed with
one of the following experimental diets for 28 days: a high
cholesterol diet (normal diet
containing 1.0% cholesterol and 5.0% lard, w/w) (control group,
n=7), a 1.0% probucol diet
(HC plus 1.0% probucol) (PB group, n=7), a 1.0%-PET diet (HC
diet plus 1.0% PET) (n=9), and a
2.0%-PET (HC diet plus 2.0% PET) (n=8). There was no
significant difference in body weight at the
end of this feeding experiment. The lag phases (Tlag, hr) in
Cu2+-induced oxidation of LDL from
these groups were control (2.5+0.8), 1.0% PET (10.6+3.7), 2.0%
PET (14.4+4.0), and PB (35.8+8.3),
respectively. Treatment with 1.0% PET, 2.0% PET, and 1.0%
probucol led to 4.2 , 5.8, and 14.3
fold increases in lag phase. The content of a-tocopherol in
LDL from 2.0% PET group (7.6+2.2
molecules/LDL) was significantly higher than those from control
(5.0+0.9 molecules/LDL), 1.0% PET
group (5.5+1.5 molecules/LDL), and 1.0% probucol group (5.3+1.3
molecules/LDL) (p<0.05). The
content of polyunsaturated fatty acids (PUFA) in LDL from 2.0%
PET group (1012+153 molecules/LDL)
was significantly low than those from control (1321+349
molecules/LDL) (p<0.05) and 1.0% probucol
(1498+189 molecules/LDL) (p<0.001) groups. Results from this
animal study firmly demonstrated that
feeding with aqueous extract of Pu-Erh-Tou tea reduced
oxidative susceptibility of LDL from
experimental animals.
This study concludes that Pu-Erh-Tou tea contains strong antioxidants
that can scavenge DPPH radical and inhibit LDL oxidation in
vitro and in vivo. It suggests that
uptake of Pu-Erh-Tou tea may have preventive effect in
atherosclerosis and coronary heart disease.
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