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INVESTIGATION OF THE HEPATOPROTECTIVE EFFECT OF ANACARDIUM IN
AN ETHANOL-INDUCED HEPATITIS MODEL
Akhmadova Maftuna
Master,
National University of Uzbekistan
Yunusova Muslima
Acting associate professor of the
National University of Uzbekistan, PhD
Seit-Asan Lenara
Research Intern at
National University of Uzbekistan
Mukhamedova Mukambar
Lecturer at the Lyceum at TashPMI
Abstract.
This article presents the results of experimental studies on the hepatoprotective effects
of the plant-derived polyphenolic compound anacardine in models of acute ethanol-induced liver
injury. The relevance of the research lies in the limited availability and efficacy of local
hepatoprotective drugs in the global pharmaceutical market, highlighting the need for effective,
low-toxicity, and affordable plant-based alternatives. The study was conducted in accordance with
international ethical standards using Wistar rats, and liver injury was induced using 33% ethanol.
Anacardine was administered orally and intraperitoneally in various doses. The therapeutic
efficacy was assessed by biochemical markers such as ALT, total protein, lipid peroxidation
products (DCs and TBARS), and hepatoprotection coefficients. The results demonstrated that an
oral dose of 100 mg/kg and an intraperitoneal dose of 5 mg/kg of anacardine showed the most
significant improvement in liver function indicators, suggesting optimal hepatoprotective effects.
Compared to standard treatment with Karsil, anacardine exhibited comparable or even superior
results in some parameters. The findings support the potential use of anacardine as a natural
hepatoprotective agent in liver injury associated with alcohol toxicity.
Keywords:
anacardine, hepatoprotection, polyphenols, ethanol-induced liver injury, biochemical
markers, experimental hepatology, oxidative stress.
Introduction.
At present, the share of effective domestic hepatoprotectors in the global
pharmaceutical market is small, and similar foreign medicinal products also constitute a limited
proportion. Taking this into account, there is a growing need to discover new agents that can
enhance liver resistance to toxic damage. In this context, preference should be given to herbal
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preparations, which are generally characterized by low toxicity and a sufficiently broad and
effective therapeutic action.
Materials and Methods.
The studies were conducted in accordance with international
recommendations of the European Convention for the protection of vertebrate animals used in
experimental and other scientific purposes, using 240 mature white Wistar rats of both sexes,
weighing between 170–280 grams [1].
Acute alcoholic liver damage was induced by intraperitoneal administration of a 33% ethanol
solution. The experimental use of the polyphenol anacardine was performed using both oral and
intraperitoneal routes of administration in the model animals.
The studied anacardine polyphenol was administered orally at doses of 100, 300, and 500 mg/kg
div weight twice daily for 12 days through gastric intubation, and intraperitoneally at doses of 5,
15, and 25 mg/kg twice daily for 12 days. It should be noted that the tested polyphenol was
administered 5 days prior to the introduction of the hepatotoxin (carbon tetrachloride or ethanol),
and continued during the 7 days of toxin administration — that is, the polyphenol was given 1
hour before the injection of carbon tetrachloride or ethanol [3,7].
The functional activity of the liver was evaluated based on the duration of sleep in animals [4],
which reflects the condition of the microsomal system involved in the metabolism of xenobiotics,
particularly sodium ethaminal. The experiment was conducted according to the method of V.V.
Gatsura [7]. After administering the investigational compound for 14 days to ethanol-induced
model animals, sodium ethaminal was injected intraperitoneally at a dose of 40 mg/kg. The sleep
duration (in the lateral position) was recorded in minutes. Statistical results were processed and
expressed as the arithmetic mean (M) and its standard error (m).
Sodium ethaminal and the studied anacardin polyphenol were administered via the oral route at
various doses (100, 300, and 500 mg/kg), and intraperitoneally at different doses (5, 15, 125
mg/kg). On the 14th day of administration, under conditions of acute toxic liver injury induced by
ethanol solution, the compounds were introduced intraperitoneally at a dose of 40 mg/kg [6].
Animals receiving the same amount of purified water served as the control group.
Results
. According to the obtained results, compared to the control group, administration of
anacardin resulted in a significant and reliable reduction in sleep duration, with a maximum
reduction observed at the 100 mg/kg dose — 55.7%. In our study, the focus was on determining
the optimal therapeutic dose of the investigational compound that would normalize disrupted
biochemical indicators in hepatocytes under ethanol-induced liver injury conditions.
In our experiments, the content of diene conjugates was initially determined. The concentration of
diene conjugates was expressed in μmol/L. According to the results obtained in ethanol-induced
liver pathology, when the dose was increased to 300 mg/kg, the total protein concentration in
blood serum significantly increased by 22% compared to the control group, while the levels of
DC (diene conjugates) and TBARS (thiobarbituric acid-reactive substances) decreased
significantly by 102.29% and 131.22%, respectively. However, this effect was lower than that
observed at the 100 mg/kg dose.
Further increasing the dose of anacardic acid to 500 mg/kg did not produce any additional positive
effect on these parameters and did not result in statistically significant changes. Based on the
hepatoprotection coefficient value and the degree of biochemical marker recovery, the highest
coefficient (49%) was observed in animals receiving 100 mg/kg of anacardic acid. This value was
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reliably higher than those observed at doses of 100, 300, and 500 mg/kg (which were 24%, 22%,
and 18%, respectively).
In the next stage of the study, to determine the effective dose of anacardic acid when administered
intraperitoneally and to confirm its efficacy at 5 mg/kg, the dynamics of biochemical marker
changes were investigated in a model of ethanol-induced toxic liver injury at different doses (5,
15, and 25 mg/kg).
When the dose was increased to 15 mg/kg, the total protein level in blood serum rose by 22%
compared to the control, while the levels of DC and TBARS decreased significantly by 102.29%
and 131.22%, respectively. However, these values were still lower than those observed at the 5
mg/kg dose. A further increase in the dose to 25 mg/kg did not enhance the effects and did not
lead to significant changes.
According to the hepatoprotection coefficient, taking into account the recovery of biochemical
parameters, the highest coefficient (49%) was recorded in animals that received anacardic acid at
a dose of 5 mg/kg. This was reliably higher than the coefficients observed at doses of 15 and 25
mg/kg (which were 24% and 22%, respectively).
The general parameters of the obtained data, including integral indicators of survival, detailed
biochemical analysis of serum and liver, as well as data calculated by the hepatoprotection
coefficient, allow suggesting a dose of 5 mg/kg of anacardine administered intraperitoneally as an
effective therapeutic dose.
Conclusion.
In ethanol-induced hepatitis models, comparison of the hepatoprotective effect of
anacardine with Karsil showed that, relative to the control group, the concentration of diene
conjugates in blood serum was corrected by 49%, and the content of thiobarbituric acid reactive
substances (TBARS) was reduced by 36.4% in blood serum and by 41.7% in liver tissue. The
increase in alanine aminotransferase (ALT) activity, as a marker of cytolysis, and the decrease in
total protein levels were also normalized under the influence of the administered compound.
References:
1.
Алимова C.B. Выживаемость и особенности алкогольных циррозов печени при
аллельных
вариантах
алкогольокисляющих
ферментов:
автореф.
дис.канд.
мед.наук/С.В.Алимов. — Москва, 2005. -28 с.
2.
Астахин A.B. Концентрация фактора некроза опухоли-a при хронических
гепатитах/А.В.Астахин,
Б.Н.Левитан,
О.С.Дудина
//
Эксперим.
и
клинич.
гастроэнтерология. - 2003. — №1. - С. 122.
3.
Буеверов А.О. Оксидативный стресс и его роль в повреждении печени//Рос.журн.
гастроэнтеологии, гепатологии, колопроктологии. -2002.-№4.-С. 21-25.
4.
Венгеровский А.И. Методические указания по изучению гепатозащитной активности
фармакологических
веществ/А.И.Венгеровский,
И.В.Маркова,
А.С.Саратиков//
Руководство
по
экспериментальному
(доклиническому)
изучению
новых
фармакологических веществ / под ред. Р.У. Хабриева. - Москва, 2005. - С.683-691.
5.
Владимиров, Ю.А. Перекисное окисление липидов в биологических мембранах/Ю.А.
Владимиров, А.И. Арчаков.– М.: Наука, 1972. – 252 с.
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RESEARCH & DEVELOPMENT
SJIF 2019: 5.222 2020: 5.552 2021: 5.637 2022:5.479 2023:6.563 2024: 7,805
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322
6.
Гаврилов В.Б. Спектрофотометрическое определение содержания гидроперекисей
липидов в плазме крови/В.Б Гаврилов, М.И. Мишкорудная//Лаб.дело.–1983.-№ 3.–С.33-35.
7.
Чесноковa Н.П., Ледванов М.Ю.. Активация свободноадикального окисления –
эфферетное звено типовых патологических процессов//Под ред. Н.П. Чесноковой, М.Ю.
Ледванова- Саратов: Изд- во Саратов. мед. ун-та. 2006. – C. 177.
