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Department of Applied Biological Chemistry, Faculty of Agriculture, Shizuoka University, Shizuoka 422-8529, Japan and * Department of Food and Nutrition, Faculty of Human Life Science, Osaka City University, Osaka 558-8585, Japan
2To whom correspondence should be addressed.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • INDEXING • D-galactosamine • liver injury • green tea • dietary fiber • rats
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). Teas contain relatively large amounts of catechins (tea
tannins) in addition to caffeine. A number of studies have shown that
teas or tea catechins have a wide range of biological effects, such as
antioxidation (Matsuzaki and Hara 1985
), antimutation
(Kada et al. 1985
), anticarcinogenesis (Fujiki et al. 1996
), antibiotic action (Toda et al. 1989
),
antihypercholesterolemia (Muramatsu et al. 1986
),
antihypertension (Hara and Tonooka 1990
),
antihyperglycemia (Shimizu et al. 1988
) and
anti-inflammatory action (Sagesaka et al. 1996
).
Furthermore, we recently demonstrated that
D-galactosamine-induced liver injury could be
suppressed by dietary supplementation with a powder of a green tea
extract (Sugiyama et al. 1998
). Liver injury is caused
by different agents, such as viruses, chemicals, alcohol, and
auto-immune diseases. It was pointed out that liver injury induced
by D-galactosamine resembles that induced by the
H-1 strain virus, one of two serologic types of rat virus, in its
symptoms (Keppler et al. 1968
).
D-Galactosamine is thought to induce
hepatotoxicity by inhibiting the synthesis of RNA and protein through a
decrease in cellular UTP concentration, which finally leads to the
necrosis of liver cells (Decker and Keppler 1974
). The
extent of liver injury can be easily estimated by measuring the
activities of certain plasma enzymes, e.g., alanine aminotransferase
(ALT)3
and aspartate aminotransferase (AST). It would be interesting to know
what types of beverages are more effective than others in protecting
the liver from injury, but little information is available It is also
unclear by what constituent(s) and by what mechanism(s) green tea
exerts its liver injury-preventive effect. In this study, we investigated the effects of dietary supplementation with different types of beverages on D-galactosamine-induced liver injury in rats, as assessed by ALT and AST activities. The effects of five fractions, which were prepared from a green tea extract by successive extraction with different organic solvents, were also investigated to determine what type of constituents contributes to the effect of green tea. Furthermore, the effects of different types of dietary fibers and short-chain fatty, acids such as acetate, propionate, and butyrate, on D-galactosamine-induced liver injury were investigated to confirm the effect of dietary fibers because the soluble dietary fiber fraction of green tea was found to have a liver injury-preventive effect.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Various types of teas, instant coffee and cocoa were obtained from a market (Shizuoka City, Japan). The green tea (Sen-cha) and roasted green tea (Houji-cha) we used were made in Japan, the puerh tea and oolon tea in China, the black tea in England, and the instant coffee and cocoa in Japan. Sodium alginate, pectin (lemon), and inulin were obtained from Wako Pure Chemical (Osaka, Japan), and cellulose, glucomannan (konjak mannan), and guar gum were obtained from Oriental Yeast (Tokyo, Japan), Shimizu Shokuhin (Shimizu, Japan) and Sigma Chemical (St. Louis, MO), respectively. Corn hemicellulose (water-soluble type) was supplied by Nihon Shokuhin Kako (Tokyo, Japan), and chitin and chitosan supplied by Yaizu Suisan Kagaku (Yaizu, Japan). D-Galactosamine was obtained from Sigma. Authentic tea catechins and caffeine for HPLC analysis were obtained from Funakoshi (Tokyo, Japan) and Sigma, respectively. Sodium acetate, sodium propionate, and sodium butyrate were obtained from Wako. Mineral and vitamin mixtures were obtained from Oriental Yeast.
Extraction of teas, fractionation and analysis of constituents.
Teas were extracted as follows: 10 volumes (v/wt) of boiling water was
added to each tea, let stand for 30 min at room temperature, and the
extract was filtered through five sheets of gauze. The extract was
lyophilized and powdered with a mixer. The dry matter thus obtained
were 23–24 g per 100 g for five types of teas. The powder of a
green tea extract was further fractionated into five fractions by
successive extraction with organic solvents, such as chloroform, ethyl
acetate, n-butanol, and 70% (v/v) ethanol (Fig. 1
), according to Matsuzaki and Hara (1985)
and Sagesaka et al. (1994)
with slight modifications. A relatively large amount of soluble
fiber fraction (fraction V) was likewise prepared to examine its
dose-dependent effect. The concentrations of caffeine and catechins
in a green tea extract and fractions I and II (Fig. 1)
were measured by
HPLC (Model LC 10A; Shimadzu, Kyoto, Japan) using an
octadecylsilyl column (6 x 150 mm; Shimadzu) according to
Terada et al. (1987)
. The sugar content of fraction V (Fig. 1)
was
determined by a phenol-sulfate method using
D-glucose as a standard (Dubois et al. 1956
).
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Five-wk-old male Wistar rats, weighing 90–100 g, were obtained from
Japan SLC (Hamamatsu, Japan). The rats were individually housed in
hanging, stainless steel, wire cages and kept in an isolated room at a
controlled temperature (23–25°C) and ambient humidity (50–60%).
Lights were maintained on a 12-h light-dark cycle (lights on from
0600 to 1800 h). Animals were acclimated to the facility for 4 or
5 d and given free access to water and a commercial stock diet
(Type MF; Oriental Yeast). The composition of the control diet was as
follows (g/kg): casein, 250; corn starch, 401; sucrose, 200; corn oil,
50; mineral mixture (American Institute of Nutrition 1977
), 35; vitamin mixture (American Institute of Nutrition 1977
), 10; choline bitartrate, 4; and cellulose, 50.
Supplements were added to the control diet at the expense of cellulose.
Rats were given free access to the experimental diets, and body weight
and food consumption were measured daily.
In this study, six separate experiments were conducted. In experiment 1, 78 rats were divided into nine groups and fed the control diet or diets supplemented with the powder of one of each tea extract, instant coffee, or cocoa at a level of 30 g/kg. In experiment 2, 75 rats were divided into eight groups and fed the control diet or diets supplemented with the powder of a green tea extract (30 g/kg diet) or one of each fraction from a green tea extract. Each fraction was added to the diet to make it comparable to the addition of powdered green tea extract on the basis of percentage distribution of each fraction. In experiment 3, 50 rats were divided into six groups and fed the control diet or diets supplemented with a soluble dietary fiber fraction (fraction V) at levels of 1, 2, 4, 6 or 10 g/kg. In experiment 4, 90 rats were divided into 11 groups and fed the control diet or diets supplemented with different types of dietary fibers at a level of 30 g/kg. In experiment 5, 42 rats were divided into five groups and fed the control diet or diets supplemented with guar gum at levels of 5, 10, 30, or 50 g/kg. In experiment 6, 34 rats were divided into four groups and fed the control diet or diets supplemented with sodium acetate, sodium propionate, or sodium butyrate at levels of 20.8, 19.7, or 19.0 g/kg. These addition levels corresponded to a net amount of short-chain fatty acids of 15 g/kg diet.
After feeding the experimental diets for 14 d, D-galactosamine was injected intraperitoneally at a dose of 350 mg/kg body weight between 1400 and 1440 h. Untreated rats were injected with saline. After the injection (22 h), rats were killed by decapitation between 1200 and 1240 h to obtain blood and liver. Rats were not starved either before and after the injection of saline or the drug. Blood plasma was separated from heparinized, whole blood by centrifugation at 2000 x g for 20 min at 4°C; the plasma and liver were stored at -30°C until analyses. The experimental design was approved by the Laboratory Animal Care Committee of the Faculty of Agriculture, Shizuoka University.
Biochemical analysis.
The activities of plasma ALT and AST were measured with a kit
(Transaminase C II-Test, Wako). The enzyme activity was expressed
as µmol/(min·L plasma) at 25°C. In some of the rat groups of
experiment 1, several variables of the liver and plasma were measured.
Whole liver was minced and divided into two portions. The water content
of the liver was determined by lyophilizing one portion of the liver.
Another portion was homogenized in 4 volumes (v/wt) of ice-cold
saline, and the protein, nucleic acids, and glycogen content of the
homogenates were determined. Protein was measured by the method of
Lowry et al. (1951)
using bovine serum albumin as a standard. RNA and
DNA were separated by the method of Schneider (1946)
and measured
spectrophotometrically. The optical density of 0.286 at 260 nm was
assumed to represent nucleic acid concentration of 10 mg/L. Glycogen
was measured by the anthrone method (Stifter et al. 1950
). Plasma glucose concentration was measured enzymatically
with a kit (Glucose C II-Test; Wako).
Statistical analysis.
Results were expressed as mean ± SEM . Data were
analyzed by one-way ANOVA, and the difference between means were
tested at P < 0.05 using Duncan's multiple range
test (Duncan 1957
) when the F value was
significant at P < 0.05. Simple correlation
between variables was calculated by linear regression analysis.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Most of the beverages, except for cocoa, depressed growth compared to
D-galactosamine-injected control rats, whereas
food intake was reduced by green, puerh, and black teas compared to
D-galactosamine-injected control rats
(Table 1). Relative liver weights were significantly lower in
D-galactosamine-injected control rats than in
saline-injected control rats. Most of the beverages, except for
cocoa, partially prevented the decrease in liver weight caused by
D-galactosamine injection. Activities of plasma
ALT and AST were dramatically enhanced by
D-galactosamine injection. The increases in
these enzyme activities were significantly suppressed by all of the
beverages tested, although the magnitude of the effect varied. There
was a significant correlation between the activity of ALT and AST among
the nine groups (r = 0.975, P < 0.001,
n = 9). As a whole, certain types of teas, such as
green, puerh, and black, had a greater effect than coffee and cocoa.
The effects of green tea on liver components and plasma glucose
concentration were measured (Table 2). D-Galactosamine injections, compared to
saline injections, significantly enhanced the water and DNA contents of
the liver and, conversely, reduced protein, glycogen, and RNA contents;
the ratio of protein or RNA to DNA; and plasma glucose concentration.
Dietary supplementation with a green tea extract partially prevented or
tended to prevent these effects of
D-galactosamine.
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The HPLC analysis showed that a green tea extract contained 6.2 g
of caffeine and 27.3 g of catechins per 100 g. Fraction I
(Fig. 1)
contained 87.5 g caffeine and a trace amount of catechins
per 100 g, whereas fraction II contained 1.5 g caffeine and
83.2 g catechins per 100 g. These data confirmed that the
major constituents of fractions I and II were caffeine and catechins,
respectively. The sugar content of fraction V was at least 95 g
per 100 g, indicating that this fraction was composed of
polysaccharides. Consistent with the results of experiment 1, body
weight gain was significantly lower in rats fed a green tea extract
than in rats fed the control diet (Table 3). Of the five fractions prepared from the green tea extract, only
fraction I caused significant depressions of body weight gain and food
intake. Relative liver weights were higher in rats fed diets
supplemented with a green tea extract or each fraction, except for
fraction II, than in D-galactosamine-injected
control rats. Fractions II, III, IV, and V had suppressive effects on
D-galactosamine-induced enhancement of ALT and
AST activities, although the intensity of the effect of fraction II on
ALT activity was significantly smaller than those of fractions III and
IV. Because fraction V was found to be relatively pure, the
dose-dependent effect of this fraction (soluble tea dietary fibers)
was investigated. The minimum dose that had a significant effect was 2
g/kg diet for both ALT and AST activities (Fig. 2
).
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The growth of rats was slightly depressed only by chitosan, and food
intake was slightly lowered by hemicellulose, chitosan, guar gum, and
glucomannan compared to D-galactosamine-injected
control rats (P < 0.05; Table 4). None of the dietary fibers tested affected relative liver
weight. Most of the dietary fibers, except for cellulose, suppressed
the D-galactosamine-induced enhancement of
plasma ALT and AST activities, with different amplitudes of the effect.
Because guar gum had the strongest effect, this fiber was further
investigated. Guar gum suppressed the enhancement of plasma enzyme
activities in a dose-dependent manner (Fig. 3
); the effect was significant, even at a low addition level (5 g/kg
diet). Because certain types of dietary fibers are assimilated by
intestinal microflora to produce short-chain fatty acids, such as
acetate, propionate, and butyrate, the effect of dietary
supplementation with these acids on
D-galactosamine-induced liver injury was
assessed to study the mechanism by which dietary fibers suppress liver
injury. None of the short-chain fatty acids tested depressed the
growth or food intake of animals (data not shown). The plasma
ALT activities were 1325 ± 94 [µmol/(min·L), control,
n = 10], 864 ± 30 (acetate, n = 8), 1365 ± 74 (propionate, n = 8), and 1471
± 98 (butyrate, n = 8), and the AST activities
were 3412 ± 267 (control), 2847 ± 200 (acetate), 3851
± 222 (propionate), and 3829 ± 232 (butyrate). In both
enzyme activities, only acetate had significantly suppressive effects
(P < 0.05) compared to the control group.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). This was also the case for the present study. It should
be noted, however, that suppression of growth and food intake, per se,
would not be associated with the liver injury-preventive effect of
beverages because the caffeine-containing fraction (fraction I) did
not suppress liver injury while it did depress the growth of the rats.
The reported D-galactosamine-induced changes in
the concentration of liver components, such as RNA, protein, and
glycogen (Decker and Keppler 1974
; Keppler et al. 1968
), were also observed in the present study. The fact that
green tea normalized, or tended to normalize, the decreased
concentrations of these variables also supports that green tea could
protect against the hepatotoxicity of
D-galactosamine.
In the present study, we focused our attention on the constituents of
green tea because green tea was one of the most effective beverages in
alleviating D-galactosamine-induced liver
injury. For this purpose, a green tea extract was separated into five
fractions by successive extraction with organic solvents, and the
effect of each fraction was investigated. Several fractions had
preventive effects on D-galactosamine-induced
liver injury. It is apparent that caffeine had no preventive effect on
liver injury. Fraction II, which contained tea catechins as major
constituents, had a significant effect, but the extent of the effect
generally was smaller than that of some other fractions (Table 3)
.
These results indicate that the major part of the effect of green tea
cannot be ascribed to tea catechins. In contrast, Hikino et al. (1985)
showed that, when added to a medium of primary cultured rat
hepatocytes, catechins had a preventive effect on
D-galactosamine- and carbon
tetrachloride-induced hepatotoxicity. Recently, Miyagawa et al. (1997)
also reported that tea catechins could protect against the
cytotoxicity of 1,4- naphthoquinone in primary cultured rat
hepatocytes. It seems worthwhile to note that the intestinal absorption
of tea catechins is very low in humans (Nakagawa et al. 1997
, Unno et al. 1996
). Nakagawa et al. (1997)
estimated the absorption of (-)-epigallocatechin gallate and
(-)-epigallocatechin to be only 0.2–2% and 0.2–1.3% of the amount
of administered, respectively. The low absorbabilities of catechins
suggest that the effect of tea catechins in vivo may be far smaller
than that expected from the results obtained in vitro or in cells in
culture. However, the effect of tea catechins on liver injury must be
further studied by using pure tea catechins to obtain conclusive
results. Fractions III, IV, and V were found to have relatively strong
effects on D-galactosamine-induced liver injury.
Fraction III, which was prepared by extracting with
n-butanol, was shown to contain tea saponins and flavonoids
(Sagesaka et al. 1994
), whereas fraction IV, which was
soluble in 70% ethanol, contains water-soluble compounds of low
molecular weights, such as free sugars, amino acids, and
oligosaccharides. Recently we found that glycosidic flavonoids included
in fraction III had a liver injury-preventive effect (Wada et al. 1999
), but the entity responsible for the effect of
fraction IV has not yet been elucidated. In contrast, fraction V was
relatively pure and was composed of soluble dietary fibers
(polysaccharides). With regard to this fraction V, Shimizu et al. (1988)
have already isolated soluble polysaccharides from an
extract of green tea (Ban-cha), which had a hypoglycemic effect in
streptozotocin-induced diabetic rats. They showed that the
molecular weight was ~40 kDa, and the constituting sugars were
arabinose, D-ribose, and
D-glucose (5.1:4.7:1.7, wt/wt). These soluble
polysaccharides are considered to be contained in fraction V of the
present study.
The present study demonstrated that in addition to tea soluble dietary
fibers, many other dietary fibers also have preventive effects on
D-galactosamine-induced liver injury. These
results suggest that prevention of liver injury may be one of the
important physiological effects of dietary fibers. It is interesting
that Wang et al. (1995)
have shown that dietary supplementation with
free galactose or galactose-containing oligosaccharides, such as
lactose, lactulose, raffinose, and some other galactooligosaccharides,
had a preventive effect on
D-galactosamine-induced liver injury in rats.
Based on these results, they concluded that the galactose residue of
oligosaccharides participates in the effect. This might be applied to
the effect of polysaccharides. However, this assumption cannot explain
why several dietary fibers, which do not contain galactose, e.g.,
chitin, chitosan, glucomannan, alginate, and inulin, also suppressed
D-galactosamine-induced liver injury. Therefore,
it is possible that dietary fibers exert their suppressive effects on
D-galactosamine-induced liver injury through
both galactose-dependent and galactose-independent mechanisms.
In terms of the physiological and nutritional effects of dietary
fibers, the latter mechanism appears to be more interesting than the
former because D-galactose may alleviate
D-galactosamine-induced liver injury simply by
competing with D-galactosamine in some metabolic
processes.
At present, the mechanism of the galactose-independent liver
injury-preventive effect of dietary fibers is unclear. Recently,
Hase et al. (1996)
have demonstrated that celosian, an acidic
polysaccharide isolated from the seeds Celosia argentea, had
a liver injury-preventive effect in different liver injury models,
including that caused by the administration of
D-galactosamine and bacterial lipopolysaccharide
(LPS). In their study, celosian was administered to mice and rats
intraperitoneally or subcutaneously, whereas in the present study
fibers were added to the diet and fed to rats. So, the possibility that
the mechanism of the liver injury-preventive effect of dietary
fibers may be different from that of celosian cannot be ruled out. In
our investigation, it seems unlikely that dietary fibers suppressed
liver injury simply by preventing the absorption of
D-galactosamine because fibers and
D-galactosamine were administered by different
routes. A number of studies have shown that certain types of dietary
fibers can be assimilated by intestinal microflora to produce
short-chain fatty acids, such as acetate, propionate, and butyrate
(Eastwood 1992
). With regard to this ability of
intestinal microflora, it is interesting that, in the present
study, acetate was found to have a liver injury-preventive
effect when added to the diet. This finding can be taken to support the
idea that certain dietary fibers may elicit their liver
injury-preventive effects, at least in part, via specific
short-chain fatty acid, e.g., acetate, one of the results of the
fermentation of dietary fibers by intestinal microflora. However, this
assumption must be further examined.
D-Galactosamine is usually used in combination
with other hepatotoxic substances, such as LPS, in mice. In the present
study, we used D-galactosamine alone to cause
liver injury because rats are much more sensitive to
D-galactosamine than are mice (Galanos et al. 1979
). It should be noted, however, that in liver injury
caused by D-galactosamine and LPS, an
inflammatory response is initiated by LPS, but not by
D-galactosamine;
D-galactosamine is thought to increase the
sensitivity of hepatocytes to LPS by inhibiting the synthesis of
acute-phase proteins (Wang and Wendel 1990
). It was
postulated that tumor necrosis factor 
(TNF-), released mainly
from activated macrophages, acts as a mediator for several types of
experimental liver injury, including that caused by
D-galactosamine and LPS, through the induction
of the transcription of proinflammatory genes (Bradham et al. 1998
). Actually, TNF- could substitute for LPS in
D-galactosamine-sensitized mice (Tiegs et al. 1989
), supporting the central role of TNF- in
LPS-induced hepatic injury. It is unclear whether TNF- also
plays a critical role in the model of rat liver injury caused by
D-galactosamine alone, but further studies on
the effect on TNF- should help to elucidate the mechanism of the
liver injury-preventive effect of beverages.
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FOOTNOTES |
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3 Abbreviations used: ALT, alanine
aminotransferase; AST, aspartate aminotransferase; LPS,
lipopolysaccharide; TNF-, tumor necrosis factor .
Manuscript received July 28, 1998. Initial review completed August 28, 1998. Revision accepted March 10, 1999.
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 P. He, Y. Noda, and K. Sugiyama Green Tea Suppresses Lipopolysaccharide-Induced Liver Injury in D-Galactosamine-Sensitized Rats J. Nutr., May 1, 2001; 131(5): 1560 - 1567. [Abstract] [Full Text]
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