17 research outputs found
Inadequate fat diet
Aim. To determine the main factors of inadequate fat diet (IAFD) and indicate the ways of their change.Methods. Analysis and generalization of existing scientific literature data and the results of our own research.Results. The following factors of IAFD have been identified:1) excess fat in the diet;2) an excess of palmitic acid in dietary fats;3) an excess of linoleic acid in dietary fats;4) consumption of thermoperoxide fats;5) deficiency of Ο-3 polyunsaturated fatty acids (PUFA).Conclusion. IAFD is a cause of metabolic and neuropsychiatric disorders underlying non-communicable diseases
Effect of an antidisbiotic agent on the biosynthesis of fatty acids of liver lipids of rats which received palm oil on the background of dysbiosis
Background. To determine the effect of antidysbiotic agent on the biosynthesis of fatty acids of lipids in the liver of rats fed a high-fat diet (HFD) with palm oil against the background of dysbiosis. Methods. The HFD contained 15% palm oil. In a biological experiment, white rats were used, divided into 4 groups: the 1st group received a fat-free diet (FFD), the 2nd, 3rd, and 4th received HFD. In rats of the 3rd and 4th groups, dysbiosis was reproduced using lincomycin. Rats of the 4th group from the first day of the experiment received an antidysbiotic agent (inulin + quercetin, ADA) with food. The duration of feeding is 39 days. Liver lipids were divided into 3 fractions: neutral lipids (NL), phospholipids (PL), and free fatty acids (FFA). The fatty acid composition of the fractions was determined by gas chromatography. The βactivitiesβ of fatty acid synthase, palmitic acid elongase, and stearylCoA- desaturase (SCD18 and SCD16) were determined. Results. The presence of all classes of fatty acids (FA) in the liver lipids of rats treated with FFD was established. Consumption of HFD with palm oil increased the content of NL in the liver by 6 times (gr. 2), and in group 3 by 8 times. The introduction of ADA reduces the content of NL almost to the level of the 1st group. The content of Ο-3 polyunsaturated fatty acids (PUFA) decreases in the PL fraction in rats of the 3rd group and is restored in rats of the 4th group. In rats treated with HFD, the "activity" of synthase, SCD18 and very strongly SCD16 are reduced. Conclusion: The negative effect of palm oil on the background of dysbiosis on the biosynthesis of fatty acids in the liver, leading to hepatic steatosis and deficiency of Ο-3 PUFA, can be prevented by the use of an antidysbiotic agent
Effect of dietary fats on endogenous oleic acid biosynthesis in rat liver
Aim: Determine the effect of dietary fats with different fatty acid composition on the
biosynthesis of oleic acid and its metabolic precursors in the liver .
Methods: High linoleic sunflower oil (HLSO), high oleic sunflower oil (HOSO) and
palm oil (PO) were used. Rats were fed a semi-synthetic fat-free diet (FFD) and fat diets
containing 5 % of the above oils (instead of starch) for 30 days. Liver lipids were divided into
3 fractions: neutral lipids (NL), phospholipids (PL) and free fatty acids (FFA). The fatty acid
composition of the fractions was determined by gas chromatography. The βactivityβ of fatty
acid synthase was determined from the total content of the products of this reaction (C16:0 and
C16:1). The βactivityβ of palmitic acid elongase was determined by the ratio Π‘18:0/Π‘16:0, as well
as by the formula (Π‘18:0+Π‘18:1)/(Π‘16:0βΠ‘16:1). The βactivityβ of stearic acid desaturase (SCD1)
was determined by the ratio C16:1/C16:0 (SCD16) and by the ratio C18:1/C18:0 (SCD18).
Results: In rats treated with fat diets, the content of palmitic and oleic acids is reduced
only in the NL fraction, and to the greatest extent when consuming the diet with HLSO. The
βactivityβ of palmitic acid elongase increases significantly with the consumption of a diet with HLSO. SCD16 desaturase βactivityβ decreases with fat diet, while SCD18 desaturase
βactivityβ increases. The level of SCD18 is significantly higher than the level of SCD16.
Consumption of HLSO reduces the content of Ο-3 PUFA in rat liver lipids, while the intake of
HOSO increases it.
Conclusions: HLSO diet reduces the endogenous biosynthesis of oleic and palmitic
acids, as determined by the analysis of the rat liver NL fraction. A fat diet reduces SCD16
βactivityβ but increases SCD18 βactivityβ, especially when fed a diet with HOSO. The diet
with HLSO reduces the content of Ο-3 PUFA in liver lipids
Influence of consumption of high oleic sunflower oil on the biosynthesis of fatty acids in the liver of rats
Background. To determine the effect of consumption of high-oleic sunflower oil on
the content and biosynthesis of energy and polyunsaturated (PUFA) fatty acids in rat liver
lipids.
Methods. Rats received a semi-synthetic fat-free diet in which 5 % or 15 % starch was
replaced with high oleic sunflower oil. One group of rats received a diet with 5 % regular
(high linoleic) sunflower oil. The duration of feeding was 30 days. Liver lipids were divided
into three fractions: neutral lipids, phospholipids and free fatty acids, in which the fatty acid
composition was determined by gas chromatography. The "activity" of fatty acid synthase,
palmitic acid elongase, and stearyl-CoA desaturase (SCD18) was determined by the ratio of
fatty acid content.
Results. It was found that the largest amount (60-80 %) of fatty acids in liver lipids are
energy (C16:0 + C16:1 + C18:0 + C18:1). PUFA account for 10-30% of all fatty acids, and they are also found in the liver lipids of rats fed a free-fat diet (FFD). Fatty diets reduce the "activity"
of synthase, but increase the "activity" of elongase and desaturase. A diet with high linoleic
sunflower oil reduces the content of Ο-3 PUFA in lipids, while a diet with high oleic
sunflower oil increases it dose-dependently. Fatty diets containing high oleic sunflower oil
dose-dependently reduce the "activity" of palmitic acid desaturase (SCD16). Consumption of
high linoleic sunflower oil sharply increases the ratio of Ο-6/Ο-3 PUFA in liver lipids, while
diets with high oleic oil reduce it dose-dependently
Influence of fat-free, fat and sucrose diets on the indicators of lipid metabolism in rats
The aim. To determine the effect on lipid metabolism in the serum of rats of diets: fat-free, fat and sucrose. Materials and methods. Feeding experiments were carried out on rats divided into 3 groups: the
first received a fat-free diet (FFD), the second received a diet with 5 % sunflower oil and the third
received a diet with 50 % sucrose. The condition of lipid metabolism was assessed according to the
following indicators of blood serum: the content of triglycerides (TG), cholesterol, MDA, fatty acid
composition of neutral lipids (TG + cholesterol esters) and phospholipids. The duration of feeding was
30 days.
Results. An increase in TG levels in rats fed with oil or sucrose and a decrease in MDA levels in rats
fed a sucrose diet was found. The greatest gain in live weight was found in rats fed a fat diet. The
presence of all essential fatty acids in the blood serum lipids of rats receiving FFD and a sucrose diet
was found, and the content of Ο-3 PUFAs was the highest in rats treated with FFD.
Conclusions. Rats have endogenous sources of PUFA, including the Ο-3 series. Consumption of
sunflower oil inhibits the formation of Ο-3 PUFAs and increases the Ο-6/Ο-3 PUFA ratio by 2.5-4 times.
Consumption of sucrose increases the formation of oleic acid and decreases lipid peroxidation
Reduction of mineralizing activity of periodontal bone tissue in rats with consumption of ordinary sunflower oil
More than 20 % of people over the age of 50 suffer from osteoporosis. Lipids play an
important role in the pathogenesis of osteoporosis.
Background. To investigate the effect of ordinary (high-linoleic) sunflower oil (OSO)
on the state of periodontal bone tissue.
Methods. In 5 series of experiments, determine the mineralization activity of the
alveolar appendix of the mandible rats that were obtained with feed 5 or 15 percent of OSO
for from 22 to 75 days. Mineralizing activity was determined by the ratio of activity of
alkaline and acid phosphatase. In liver lipids (fractions of phospholipids and free fatty acids)
were determined by the content of long-chain polyunsaturated fatty acids (LCPUFA) by the
gas chromatographic method.
Results. A decrease in mineralizing activity in OSO consumption, especially when
using a feed with 15 % of OSO against a dysbiosis or metabolic syndrome. A significant (almost 10 times) is shown to reduce the content of Ο-3 PUFA in fraction of phospholipids of
the liver of rats receiving a diet with a content of OSO.
Conclusion. Sunflower oil reduces the mineralizing activity of periodontal bone tissue
by reducing the endogenous biosynthesis of Ο-3 PUFA
Therapeutic and prophylactic efficiency of polyfunctional anti-disbiotic drugs under conditions of experimental lipid intoxication
Aim: to compare the therapeutic and prophylactic efficiency (TPE) of four polyfunctional antidisbiotic drugs (PFAD) in experimental lipid intoxication. Methods: TPE was assessed by the nature of changes in blood serum levels of biochemical markers of inflammation (elastase, MDA), bacteremia (urease), nonspecific immunity (lysozyme). The following PFAD were used: Kvertulin (quercetin + inulin + calcium citrate), Lekvin (lecithin + quercetin + inulin + calcium citrate), Lekasil (lecithin + milk thistle meal + calcium citrate) and Lysozyme-forte (lysozyme + quercetin + inulin + gelatin + calcium citrate). Lipid intoxication was carried out on rats by introducing
thermal peroxide sunflower oil (TPSO) with food at a dose of 4 g/kg for 75 days. PFAD was administered from day 31 at a dose of 300 mg/kg for 45 days. Results: there was a significant increase in the level of elastase, MDA, urease and a significant decrease in the activity of lysozyme in the blood serum of rats treated with TPSO. After the introduction of all drugs, a significant decrease in the level of elastase, MDA, urease and a significant increase in the activity of lysozyme were observed. Conclusion: with lipid intoxication, a dysbiotic syndrome develops, manifested by bacteremia, a decrease in the level of nonspecific immunity and manifestations of systemic inflammation. Taking polyfunctional antidisbiotic drugs reduces bacteremia, enhances nonspecific immunity and prevents
the development of systemic inflammation. The most effective remedy turned out to be "LysozymeForte"
Influence of high-fat nutrition with different fat-acid composition of fats on lipid peroxidation processes in rat's organs and tissues
The aim. To determine the effect of high-fat diet (HFD) using fats of different fatty acid composition on the content of malondialdehyde (MDA) in the organs and tissues of rats and on catalase activity. Materials and methods. The following edible fats were used: regular (high linoleic) sunflower oil, high oleic sunflower oil, palm, butter and coconut oils at a concentration of 15 % by weight of the diet. The rats were fed for 64 days. Before euthanasia, rats were bled from v. porta and v. cava inferior. The MDA content and catalase activity were determined in blood serum, in liver homogenates, intestinal mucous membranes, in skeletal muscles, heart and brain. The antioxidant-prooxidant index of API was
calculated from the ratio of catalase activity and MDA content. Results. found that the content of the MDA in v. cava is significantly higher than v. porta. High-fat diet (HFD) increases the MDA content in all tissues except the brain, and most of all in the liver and after the consumption of high-palmitic fats (palm and butter), as well as high-linoleic sunflower oil. The exception is high oleic sunflower oil, the consumption of which does not increase the MDA content. Catalase activity reacts little to HFD. Conclusions. the liver secrete MDA into the blood. HFD increases the level of MDA in organs and tissues, except for the brain, without significantly reducing the activity of catalase. The antioxidant effect of HFD using high oleic sunflower oil can be explained by the antioxidant properties of oleic acid
Therapeutic and preventive effectiveness of oral application of phitogels βKvertulinβ, βBiotritβ and βDubovyβ in inflammatory complications in the digestive system of rats treated with thermoperoxide sunflower oil
Aim. It has been established that the consumption of thermoperoxide fats causes the
development of pathological processes in the tissues of the mouth, stomach, intestines and
liver. The purpose of this work is to determine the possibility of their normalization using oral
applications of phytogels.
Methods. Thermoperoxide oil (TPSO) was obtained by heating sunflower oil in the
presence of H2O2 at a temperature of +180 Β°C for 60 minutes. Oral TPSO applications were
made on the oral mucosa at a dose of 2.25 g/kg daily for 5 days. Used mucose-adhesive
phytogels "Kvertulin" (quercetin + inulin), "Biotrit" (juice from wheat sprout) and "Dubovy"
(extract of polyphenolic compounds from oak wood) in the form of oral applications at a dose
of 2.25 g/kg for half an hour before TPSO applications daily for 5 days. Elastase and urease activity and malonic dialdehyde (MDA) content were determined in homogenates of the
mucous membranes of the cheek, stomach, small and large intestines, as well as in the liver.
Results. Oral applications of TPSO increased the levels of MDA, elastase and urease
in the tissues of the digestive system. Applications of phytogels significantly normalized these
parameters.
Conclusions. Oral applications of TPSO cause the development of inflammation in the
digestive system, especially in the liver. Oral applications of phytogels have a protective
effect, especially "Kvertulin"
ΠΠ»ΠΈΡΠ½ΠΈΠ΅ ΠΏΠΎΡΡΠ΅Π±Π»Π΅Π½ΠΈΡ Π²ΡΡΠΎΠΊΠΎΠΎΠ»Π΅ΠΈΠ½ΠΎΠ²ΠΎΠ³ΠΎ ΠΏΠΎΠ΄ΡΠΎΠ»Π½Π΅ΡΠ½ΠΎΠ³ΠΎ ΠΆΠΌΡΡ Π° Π½Π° Π±ΠΈΠΎΡ ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»ΠΈ Π²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΡΡ ΠΈ Π·Π°ΡΠΈΡΠ½ΡΡ ΠΏΡΠΎΡΠ΅ΡΡΠΎΠ² Π² ΡΡΠ²ΠΎΡΠΎΡΠΊΠ΅ ΠΊΡΠΎΠ²ΠΈ ΠΊΡΡΡ Ρ ΡΠΊΡΠΏΠ΅ΡΠΈΠΌΠ΅Π½ΡΠ°Π»ΡΠ½ΡΠΌ Π΄ΠΈΡΠ±ΠΈΠΎΠ·ΠΎΠΌ
ΠΠ΅ΡΠ° ΡΠΎΠ±ΠΎΡΠΈ: Π²ΠΈΠ·Π½Π°ΡΠΈΡΠΈ Π»ΡΠΊΡΠ²Π°Π»ΡΠ½ΠΎ-ΠΏΡΠΎΡΡΠ»Π°ΠΊΡΠΈΡΠ½Ρ Π΅ΡΠ΅ΠΊΡΠΈΠ²Π½ΡΡΡΡ Π²ΠΈΡΠΎΠΊΠΎΠΎΠ»Π΅ΡΠ½ΠΎΠ²ΠΎΡ ΡΠΎΠ½ΡΡΠ½ΠΈΠΊΠΎΠ²ΠΎΡ ΠΌΠ°ΠΊΡΡ
ΠΈ Ρ ΡΡΡΡΠ² Π·
Π΅ΠΊΡΠΏΠ΅ΡΠΈΠΌΠ΅Π½ΡΠ°Π»ΡΠ½ΠΈΠΌ Π΄ΠΈΡΠ±ΡΠΎΠ·ΠΎΠΌ. ΠΠ°ΡΠ΅ΡΡΠ°Π»ΠΈ Ρ ΠΌΠ΅ΡΠΎΠ΄ΠΈ: Π²ΠΈΠΊΠΎΡΠΈΡΡΠΎΠ²ΡΠ²Π°Π»ΠΈ ΠΌΠ°ΠΊΡΡ
Ρ Π· Π½Π°ΡΡΠ½Π½Ρ Π²ΠΈΡΠΎΠΊΠΎΠΎΠ»Π΅ΡΠ½ΠΎΠ²ΠΎΠ³ΠΎ ΡΠΎΠ½ΡΡΠ½ΠΈΠΊΡ Ρ ΠΌΠ°ΠΊΡΡ
Ρ Π· Π½Π°ΡΡΠ½Π½Ρ Π·Π²ΠΈΡΠ°ΠΉΠ½ΠΎΠ³ΠΎ (Π²ΠΈΡΠΎΠΊΠΎΠ»ΡΠ½ΠΎΠ»Π΅Π²ΠΎΠ³ΠΎ) ΡΠΎΠ½ΡΡΠ½ΠΈΠΊΡ. ΠΠΊΡΠΏΠ΅ΡΠΈΠΌΠ΅Π½ΡΠ°Π»ΡΠ½ΠΈΠΉ Π΄ΠΈΡΠ±ΡΠΎΠ· Π²ΡΠ΄ΡΠ²ΠΎΡΡΠ²Π°Π»ΠΈ Ρ ΡΡΡΡΠ² Π·Π° Π΄ΠΎΠΏΠΎΠΌΠΎΠ³ΠΎΡ Π»ΡΠ½ΠΊΠΎΠΌΡΡΠΈΠ½Ρ. ΠΠ°ΠΊΡΡ
Ρ Π²Π²ΠΎΠ΄ΠΈΠ»ΠΈ Π΄ΠΎ ΡΠΊΠ»Π°Π΄Ρ ΠΊΠΎΠΌΠ±ΡΠΊΠΎΡΠΌΡ Π² ΠΊΡΠ»ΡΠΊΠΎΡΡΡ 10 %. Π’ΡΠΈΠ²Π°Π»ΡΡΡΡ Π³ΠΎΠ΄ΡΠ²Π»Ρ ΡΡΠ°Π½ΠΎΠ²ΠΈΠ»Π° 18 Π΄Π½ΡΠ². Π
ΡΠΈΡΠΎΠ²Π°ΡΡΡ ΠΊΡΠΎΠ²Ρ Π²ΠΈΠ·Π½Π°ΡΠ°Π»ΠΈ Π½Π°ΡΡΡΠΏΠ½Ρ Π±ΡΠΎΡ
ΡΠΌΡΡΠ½Ρ ΠΏΠΎΠΊΠ°Π·Π½ΠΈΠΊΠΈ: Π°ΠΊΡΠΈΠ²Π½ΡΡΡΡ ΡΡΠ΅Π°Π·ΠΈ, Π΅Π»Π°ΡΡΠ°Π·ΠΈ, Π»ΡΠ·ΠΎΡΠΈΠΌΠ°, ΠΊΠ°ΡΠ°Π»Π°Π·ΠΈ, Π²ΠΌΡΡΡ ΠΠΠ. Π ΠΎΠ·ΡΠ°Ρ
ΠΎΠ²ΡΠ²Π°Π»ΠΈ Π·Π° ΠΏΠΎΠΊΠ°Π·Π½ΠΈΠΊΠ°ΠΌΠΈ ΠΊΠ°ΡΠ°Π»Π°Π·ΠΈ Ρ ΠΠΠ Π°Π½ΡΠΈΠΎΠΊΡΠΈΠ΄Π°Π½ΡΠ½ΠΎ-ΠΏΡΠΎΠΎΠΊΡΠΈΠ΄Π°Π½ΡΠ½ΠΈΠΉ ΡΠ½Π΄Π΅ΠΊΡ ΠΠΠ, Π° Π·Π° ΡΠΏΡΠ²Π²ΡΠ΄Π½ΠΎΡΠ΅Π½Π½ΡΠΌ Π²ΡΠ΄Π½ΠΎΡΠ½ΠΈΡ
Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΠ΅ΠΉ ΡΡΠ΅Π°Π·ΠΈ Ρ Π»ΡΠ·ΠΎΡΠΈΠΌΠ° ΡΠΎΠ·ΡΠ°Ρ
ΠΎΠ²ΡΠ²Π°Π»ΠΈ ΡΡΡΠΏΡΠ½Ρ Π΄ΠΈΡΠ±ΡΠΎΠ·Ρ. ΠΠ°ΡΠΎΠ³Π΅Π½Π½Ρ Π΄ΡΡ Π΄ΠΈΡΠ±ΡΠΎΠ·Ρ Π²ΠΈΠ·Π½Π°ΡΠ°Π»ΠΈ Π·Π°
ΡΡΠΌΠΎΡ Π²ΡΠ΄Ρ
ΠΈΠ»Π΅Π½Ρ (Π² %) Π±ΡΠΎΡ
ΡΠΌΡΡΠ½ΠΈΡ
ΠΏΠΎΠΊΠ°Π·Π½ΠΈΠΊΡΠ² Π²ΡΠ΄ ΠΏΠΎΠΊΠ°Π·Π½ΠΈΠΊΡΠ² ΠΊΠΎΠ½ΡΡΠΎΠ»Ρ, Π° Π»ΡΠΊΡΠ²Π°Π»ΡΠ½Ρ Π΄ΡΡ β ΠΏΠΎ ΡΡΠΌΡ Π²ΡΠ΄Ρ
ΠΈΠ»Π΅Π½Ρ ΡΠΈΡ
ΠΏΠΎΠΊΠ°Π·Π½ΠΈΠΊΡΠ² Π²ΡΠ΄ ΠΏΠΎΠΊΠ°Π·Π½ΠΈΠΊΡΠ² Ρ ΡΡΡΡΠ² Π· Π΄ΠΈΡΠ±ΡΠΎΠ·ΠΎΠΌ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΠΈ: Π²ΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½ΠΎ ΠΏΡΠ΄Π²ΠΈΡΠ΅Π½Π½Ρ ΡΡΠ²Π½Ρ ΡΡΠ΅Π°Π·ΠΈ, Π΅Π»Π°ΡΡΠ°Π·ΠΈ, ΠΠΠ ΡΠ° Π·Π½ΠΈΠΆΠ΅Π½Π½Ρ ΡΡΠ²Π½Ρ Π»ΡΠ·ΠΎΡΠΈΠΌΠ° Ρ ΠΊΠ°ΡΠ°Π»Π°Π·ΠΈ Ρ ΡΡΡΡΠ² Π· Π΄ΠΈΡΠ±ΡΠΎΠ·ΠΎΠΌ. Π‘ΠΏΠΎΠΆΠΈΠ²Π°Π½Π½Ρ Π²ΠΈΡΠΎΠΊΠΎΠΎΠ»Π΅ΡΠ½ΠΎΠ²ΠΎΡ ΠΌΠ°ΠΊΡΡ
ΠΈ Π·Π½ΠΈΠΆΡΠ²Π°Π»ΠΎ ΡΡΠ²Π΅Π½Ρ ΡΡΠ΅Π°Π·ΠΈ,
Π΅Π»Π°ΡΡΠ°Π·ΠΈ, ΠΠΠ ΡΠ° ΠΏΡΠ΄Π²ΠΈΡΡΠ²Π°Π»ΠΎ ΡΡΠ²Π΅Π½Ρ Π»ΡΠ·ΠΎΡΠΈΠΌΠ° Ρ ΠΊΠ°ΡΠ°Π»Π°Π·ΠΈ. ΠΠ°ΠΊΡΡ
Π° Π· Π½Π°ΡΡΠ½Π½Ρ Π·Π²ΠΈΡΠ°ΠΉΠ½ΠΎΠ³ΠΎ ΡΠΎΠ½ΡΡΠ½ΠΈΠΊΡ Π²ΠΏΠ»ΠΈΠ²Π°Ρ Π½Π° ΡΡ ΠΏΠΎΠΊΠ°Π·Π½ΠΈΠΊΠΈ Π² Π·Π½Π°ΡΠ½ΠΎ ΠΌΠ΅Π½ΡΡΠΉ ΠΌΡΡΡ. ΠΠ°ΠΊΠ»ΡΡΠ΅Π½Π½Ρ: Π²Π²Π΅Π΄Π΅Π½Π½Ρ Π² ΠΎΡΠ³Π°Π½ΡΠ·ΠΌ Π»ΡΠ½ΠΊΠΎΠΌΡΡΠΈΠ½Ρ Π²ΠΈΠΊΠ»ΠΈΠΊΠ°Ρ ΡΠΎΠ·Π²ΠΈΡΠΎΠΊ Π΄ΠΈΡΠ±ΡΠΎΡΠΈΡΠ½ΠΎΠ³ΠΎ ΡΠΈΠ½Π΄ΡΠΎΠΌΡ, ΡΠΊΠΈΠΉ ΠΌΠΎΠΆΠ½Π° Π² Π·Π½Π°ΡΠ½ΡΠΉ ΠΌΡΡΡΠΏΠΎΠΏΠ΅ΡΠ΅Π΄ΠΈΡΠΈ ΡΠΏΠΎΠΆΠΈΠ²Π°Π½Π½ΡΠΌ Π²ΠΈΡΠΎΠΊΠΎΠΎΠ»Π΅ΡΠ½ΠΎΠ²ΠΎΡ ΡΠΎΠ½ΡΡΠ½ΠΈΠΊΠΎΠ²ΠΎΡ ΠΌΠ°ΠΊΡΡ
ΠΈ.The aim: to determine the therapeutic and prophylactic efficacy of high oleic sunflower oilcake in rats with experimental dysbiosis. Materials and methods: oilcake from seeds of high oleic sunflower and oilcake from seeds of ordinary (high linoleic) sunflower were used. Experimental dysbiosis was reproduced in rats using the antibiotic lincomycin. Oilcakes were added to the composition of mixed fodders in the amount of 10%. The duration of feeding was 18 days. In the blood serum, the activity of urease, elastase, lysozyme, catalase and the content of
MDA were determined. The antioxidant-prooxidant index of API was calculated from the indicators of catalase activity and MDA content, and the degree of dysbiosis was calculated from the ratio of the relative activities of urease and lysozyme. The pathogenic effect of dysbiosis was determined by the sum of the deviations (in %) of the markers from the control indicators. The therapeutic effect was determined (in %) by the sum of deviations from the indicators in rats with dysbiosis. Results: there was an increase in the level of urease, elastase, MDA and a decrease in the level of lysozyme and catalase in animals with dysbiosis. Consumption of high oleic oilcake
reduced the level of urease, elastase, MDA and increased the level of lysozyme and catalase. Consumption of oilcake from ordinary sunflower seeds had little effect on biochemical parameters. Conclusion: the introduction of lincomycin into the body causes the development of a dysbiotic syndrome, which can be largely prevented by the consumption of high oleic sunflower oilcake.Π¦Π΅Π»Ρ: ΠΎΠΏΡΠ΅Π΄Π΅Π»ΠΈΡΡ Π»Π΅ΡΠ΅Π±Π½ΠΎΠΏΡΠΎΡΠΈΠ»Π°ΠΊΡΠΈΡΠ΅ΡΠΊΡΡ ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ Π²ΡΡΠΎΠΊΠΎΠΎΠ»Π΅ΠΈΠ½ΠΎΠ²ΠΎΠ³ΠΎ ΠΏΠΎΠ΄ΡΠΎΠ»Π½Π΅ΡΠ½ΠΎΠ³ΠΎ ΠΆΠΌΡΡ
Π° Ρ ΠΊΡΡΡ Ρ
ΡΠΊΡΠΏΠ΅ΡΠΈΠΌΠ΅Π½ΡΠ°Π»ΡΠ½ΡΠΌ Π΄ΠΈΡΠ±ΠΈΠΎΠ·ΠΎΠΌ. ΠΠ°ΡΠ΅ΡΠΈΠ°Π»Ρ ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ: ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π»ΠΈ ΠΆΠΌΡΡ
ΠΈΠ· ΡΠ΅ΠΌΡΠ½ Π²ΡΡΠΎΠΊΠΎΠΎΠ»Π΅ΠΈΠ½ΠΎΠ²ΠΎΠ³ΠΎ ΠΏΠΎΠ΄ΡΠΎΠ»Π½Π΅ΡΠ½ΠΈΠΊΠ° ΠΈ ΠΆΠΌΡΡ
ΠΈΠ· ΡΠ΅ΠΌΡΠ½ ΠΎΠ±ΡΡΠ½ΠΎΠ³ΠΎ (Π²ΡΡΠΎΠΊΠΎΠ»ΠΈΠ½ΠΎΠ»Π΅Π²ΠΎΠ³ΠΎ) ΠΏΠΎΠ΄ΡΠΎΠ»Π½Π΅ΡΠ½ΠΈΠΊΠ°. ΠΠΊΡΠΏΠ΅ΡΠΈΠΌΠ΅Π½ΡΠ°Π»ΡΠ½ΡΠΉ Π΄ΠΈΡΠ±ΠΈΠΎΠ· Π²ΠΎΡΠΏΡΠΎΠΈΠ·Π²ΠΎΠ΄ΠΈΠ»ΠΈ Ρ ΠΊΡΡΡ Ρ ΠΏΠΎΠΌΠΎΡΡΡ
Π°Π½ΡΠΈΠ±ΠΈΠΎΡΠΈΠΊΠ° Π»ΠΈΠ½ΠΊΠΎΠΌΠΈΡΠΈΠ½Π°. ΠΠΌΡΡ
ΠΈ Π²Π²ΠΎΠ΄ΠΈΠ»ΠΈ Π² ΡΠΎΡΡΠ°Π² ΠΊΠΎΠΌΠ±ΠΈΠΊΠΎΡΠΌΠΎΠ² Π² ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²Π΅ 10 %. ΠΡΠΎΠ΄ΠΎΠ»ΠΆΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΡ ΠΊΠΎΡΠΌΠ»Π΅Π½ΠΈΡ ΡΠΎΡΡΠ°Π²ΠΈΠ»Π° 18 Π΄Π½Π΅ΠΉ. Π ΡΡΠ²ΠΎΡΠΎΡΠΊΠ΅ ΠΊΡΠΎΠ²ΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ ΡΡΠ΅Π°Π·Ρ, ΡΠ»Π°ΡΡΠ°Π·Ρ, Π»ΠΈΠ·ΠΎΡΠΈΠΌΠ°, ΠΊΠ°ΡΠ°Π»Π°Π·Ρ ΠΈ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ ΠΠΠ. ΠΠΎ ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»ΡΠΌ
Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΠΈ ΠΊΠ°ΡΠ°Π»Π°Π·Ρ ΠΈ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΡ ΠΠΠ ΡΠ°ΡΡΡΠΈΡΡΠ²Π°Π»ΠΈ Π°Π½ΡΠΈΠΎΠΊΡΠΈΠ΄Π°Π½ΡΠ½ΠΎ-ΠΏΡΠΎΠΎΠΊΡΠΈΠ΄Π°Π½ΡΠ½ΡΠΉ ΠΈΠ½Π΄Π΅ΠΊΡ ΠΠΠ, Π° ΠΏΠΎ ΡΠΎΠΎΡΠ½ΠΎΡΠ΅Π½ΠΈΡ ΠΎΡΠ½ΠΎΡΠΈΡΠ΅Π»ΡΠ½ΡΡ
Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΠ΅ΠΉ ΡΡΠ΅Π°Π·Ρ ΠΈ Π»ΠΈΠ·ΠΎΡΠΈΠΌΠ° ΡΠ°ΡΡΡΠΈΡΡΠ²Π°Π»ΠΈ ΡΡΠ΅ΠΏΠ΅Π½Ρ Π΄ΠΈΡΠ±ΠΈΠΎΠ·Π°. ΠΠ°ΡΠΎΠ³Π΅Π½Π½ΠΎΠ΅ Π΄Π΅ΠΉΡΡΠ²ΠΈΠ΅ Π΄ΠΈΡΠ±ΠΈΠΎΠ·Π° ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ ΠΏΠΎ ΡΡΠΌΠΌΠ΅
ΠΎΡΠΊΠ»ΠΎΠ½Π΅Π½ΠΈΠΉ (Π² %) ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»Π΅ΠΉ ΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ² ΠΎΡ ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»Π΅ΠΉ ΠΊΠΎΠ½ΡΡΠΎΠ»Ρ. ΠΠ΅ΡΠ΅Π±Π½ΠΎΠ΅ Π΄Π΅ΠΉΡΡΠ²ΠΈΠ΅ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ (Π² %) ΠΏΠΎ ΡΡΠΌΠΌΠ΅ ΠΎΡΠΊΠ»ΠΎΠ½Π΅Π½ΠΈΠΉ ΠΎΡ ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»Π΅ΠΉ Ρ ΠΊΡΡΡ Ρ Π΄ΠΈΡΠ±ΠΈΠΎΠ·ΠΎΠΌ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ: ΡΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½ΠΎ ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΠ΅ ΡΡΠΎΠ²Π½Ρ ΡΡΠ΅Π°Π·Ρ, ΡΠ»Π°ΡΡΠ°Π·Ρ, ΠΠΠ ΠΈ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ ΡΡΠΎΠ²Π½Ρ Π»ΠΈΠ·ΠΎΡΠΈΠΌΠ° ΠΈ ΠΊΠ°ΡΠ°Π»Π°Π·Ρ Ρ ΠΆΠΈΠ²ΠΎΡΠ½ΡΡ
Ρ Π΄ΠΈΡΠ±ΠΈΠΎΠ·ΠΎΠΌ. ΠΠΎΡΡΠ΅Π±Π»Π΅Π½ΠΈΠ΅ Π²ΡΡΠΎΠΊΠΎΠΎΠ»Π΅ΠΈΠ½ΠΎΠ²ΠΎΠ³ΠΎ ΠΆΠΌΡΡ
Π° ΡΠ½ΠΈΠΆΠ°Π»ΠΎ ΡΡΠΎΠ²Π΅Π½Ρ ΡΡΠ΅Π°Π·Ρ, ΡΠ»Π°ΡΡΠ°Π·Ρ, ΠΠΠ ΠΈ ΠΏΠΎΠ²ΡΡΠΈΠ»ΠΎ ΡΡΠΎΠ²Π΅Π½Ρ Π»ΠΈΠ·ΠΎΡΠΈΠΌΠ° ΠΈ ΠΊΠ°ΡΠ°Π»Π°Π·Ρ. ΠΠΎΡΡΠ΅Π±Π»Π΅Π½ΠΈΠ΅ ΠΆΠΌΡΡ
Π° ΠΈΠ· ΡΠ΅ΠΌΡΠ½ ΠΎΠ±ΡΡΠ½ΠΎΠ³ΠΎ ΠΏΠΎΠ΄ΡΠΎΠ»Π½Π΅ΡΠ½ΠΈΠΊΠ° ΠΌΠ°Π»ΠΎ Π²Π»ΠΈΡΠ»ΠΎ Π½Π° Π±ΠΈΠΎΡ
ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»ΠΈ. ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅: Π²Π²Π΅Π΄Π΅Π½ΠΈΠ΅ Π² ΠΎΡΠ³Π°Π½ΠΈΠ·ΠΌ Π»ΠΈΠ½ΠΊΠΎΠΌΠΈΡΠΈΠ½Π° Π²ΡΠ·ΡΠ²Π°Π΅Ρ ΡΠ°Π·Π²ΠΈΡΠΈΠ΅ Π΄ΠΈΡΠ±ΠΈΠΎΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΡΠΈΠ½Π΄ΡΠΎΠΌΠ°, ΠΊΠΎΡΠΎΡΡΠΉ ΠΌΠΎΠΆΠ½ΠΎ Π² Π·Π½Π°ΡΠΈΡΠ΅Π»ΡΠ½ΠΎΠΉ ΡΡΠ΅ΠΏΠ΅Π½ΠΈ ΠΏΡΠ΅Π΄ΡΠΏΡΠ΅Π΄ΠΈΡΡ ΠΏΠΎΡΡΠ΅Π±Π»Π΅Π½ΠΈΠ΅ΠΌ Π²ΡΡΠΎΠΊΠΎΠΎΠ»Π΅ΠΈΠ½ΠΎΠ²ΠΎΠ³ΠΎ ΠΏΠΎΠ΄ΡΠΎΠ»Π½Π΅ΡΠ½ΠΎΠ³ΠΎ ΠΆΠΌΡΡ
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