CC BY
9
13. Sanchez-Ruiz JM. Protein kinetic stability. Biophysical chemistry 2010; 148(1-3): 1-15. https://doi.Org/10.1016/j.bpc.2010.02.004
14. Seo Hyun-Ju, et al. Zinc may increase bone formation through stimulating cell proliferation, alkaline phosphatase activity and collagen synthesis in osteoblastic MC3T3-E1 cells. Nutrition research and practice 2010; 4(5): 356-361. https://doi.org/10.4162/nrp.2010.4.5.356
IiU!!!!!!!!^
ВИВЧЕННЯ ВПЛИВУ В1ТАМ1ННО- ИЗУЧЕНИЕ ВЛИЯНИЯ ВИТАМИННО-
М1НЕРАЛЬНОГО КОМПЛЕКСУ, ЩО М1СТИТЬ МИНЕРАЛЬНОГО КОМПЛЕКСА, СОДЕРЖАЩЕГО
ЦИНК L-АСПАРАПНАТ, НА СТАН ПАРОДОНТА ЦИНК L-АСПАРАГИНАТ, НА СОСТОЯНИЕ
ЩУР1В В УМОВАХ МОДЕЛЮВАННЯ ПАРОДОНТА КРЫС В УСЛОВИЯХ
ПАРОДОНТИТУ МОДЕЛИРОВАНИЯ ПАРОДОНТИТА
Шнайдер С.А., Балега М.1., Зомбор С.В., Шнайдер С.А., Балега М.И., Зомбор Е.В.,
Семенов G.I., Ткаченко е.К. Семенов Е.И., Ткаченко Е.К.
Метою дослщження було вивчення впливу Целью исследования явилось изучение влияния
втмшно-мшерального комплексу, що мютить цинк L- витаминно-минерального комплекса, содержащего цинк L-
аспарагiнат, на стан тканин пародонта щурiв в умовах аспарагинат, на состояние тканей пародонта крыс в условиях
моделювання пародонтиту за допомогою екзогенно! моделирования пародонтита с помощью экзогенной
колагенази. Втмшно-мшеральний комплекс, що мютить коллагеназы. Витаминно-минеральный комплекс,
цинк L-аспарапнат, мало позитивний вплив бшьшою содержащий цинк L-аспарагинат, оказал положительное
мiрою на кiсткову тканину пародонту. Комплекс проявив влияние в большей степени на костную ткань пародонта.
пародонтопротекторш, протизапальш, антиоксидантш Комплекс проявил пародонтопротекторные,
властивостi. противовоспалительные, антиоксидантные свойства.
Ключовi слова: цинк L-аспарапнат, моделювання Ключевые слова: цинк L-аспарагинат, моделирование
пародонтиту, колагеназа, колаген, глкозамшогакани, пародонтита, коллагеназа, коллаген, гликозаминогликаны,
ясна, юсткова тканина пародонту, щури. десна, костная ткань пародонта, крысы.
Стаття надшшла 30.09.2019 р. Рецензент Срошенко Г.А.
DOI 10.26724/2079-8334-2020-3-73-247-252
UDC (577.161.2+577.161.5).001.5:616.314.17-008.1-092.4
S. A. Schnaider. VV. I liimcniuk1. V.N. Horokhivsky i. O.V Yehemova1.
M.I. Khristova2. Ye.K. Ikachenko SE " I he Institute of Stomatology And Maxillofacial Surgery ol the N WIS of I kraine". Odesa 'Danylo Halytsky Lviv National Medical I niversity. Lviv
2Odessa National Medical I niversity. Odesa
EFFECT OF HORMONE-ACTIVE METABOLITES OF CHOLECALCIFEROL ON THE STATE OF THE ORAL CAVITY TISSUES IN RATS UNDER THE CONDITIONS OF ESTROGEN DEFICIENCY AND TRAUMATIC STRESS
e-mail: ksenianikolainko@gmail.com
The purpose of the study was to comparatively establish the effect of active metabolites of vitamin D3 on the periodontal condition of rats under conditions of experimental estrogen deficiency and traumatic stress. The experiment was carried out on 31 female breeding Wistar rats. 1st group was intact one (8 animals). The rats of the 2nd - 4th groups underwent ovariectomy and a fQnQB frUTurD GrQiQ2 wB TitrQ QiD(8 rQs); rQs Of thD3rd Old 4th grQiQ rnTUrd QJ Q QCHQQnBis qgOBst thD background of the pathogenic effect: Group 3 (8 rats) - 1-a-hydroxycholecalciferol at a dose of 0.1 ¡ig QJ dmQJ rO; E thDGrQiQ
4 (7 rats) - 24,25-hydroxycholecalciferol at a dose of 1.25 ¡ig per day/rat. At the time of sacrifice, the animals were 15 months old. Under the influence of risk factors for periodontitis, protective properties of hormone-active metabolites of vitamin D3 were observed. They were expressed in inhibition of lipid peroxidation processes in the oral mucosa of rats, as well as periodontal protective effects when using 24,25-hydroxycholecalciferol.
Key words: vitamin D3 metabolites, estrogen deficiency, traumatic stress, periodontal protection properties, antioxidant effect, rats.
The study is a fragment of the research project "The effect of hypoxia on the processes of collagen formation and mineralization in models of dental pathology and correction of these disorders", state registration No. 0118U006963.
Vitamin D3 or cholecalciferol, which realizes its action in the organism through active metabolites - 25OHD3, 1,25(OH)2D3 and 24,25(OH)2D3, is directly involved in the bone tissue metabolism. 1,25(OHhD3 or calcitriol, is the most biologically active metabolite of vitamin D3. With a deficiency of calcium and phosphorus, the metabolism of 25OHD3 follows the formation of 1,25 (OH) 2D3, which is catalyzed by the enzyme 1-a-hydroxylase, which is present in the mitochondria of renal tubular epithelial cells. With an increased or normal concentration of calcium and phosphorus in the blood serum, an alternative metabolite, 25OHD3 - 24,25(OH)2D3, is formed with 24-hydroxylase [10]. The fundamental
© S.A. Schnaider, V.V. Humeniuk, 2020
difference in the effects of 1.25 (OH) 2D3 from 24,25 (OH)2D3 consists in the fact that in the first place is its resorption effect on the bone. At the same time, both metabolites have practically the same activity in relation to the absorption of calcium in the intestine. 24,25(OHhD3 effects under physiological conditions, it ensures the calcium absorption in the intestine and utilization in the processes of mineralization and osteogenesis of bone tissue.
Recently, it has been shown that vitamin D3 can affect the functioning of many organs and body systems. In addition to the well-known vitamin D3 participation in the regulation of calcium and phosphorus metabolism and related effects in the processes of bone tissue remodeling, vitamin D3 also has an immunomodulatory, anti-inflammatory, antiproliferative effect and is able to prevent tumor cell transformation [5]. Molecular mechanisms that provide the cytoprotective properties of vitamin D3 can be realized both through genomic regulation, which mechanism mainly corresponds to the steroid hormone effects, and through non-genomic effects, including its influence on the expression of signaling proteins, cellular metabolism, inflammatory processes, and oxidative stress [11].
Vitamin D3 is critical for the functioning of a wide variety of organ systems, and its deficiency contributes not only to low bone mineral density, osteoporosis, osteopenia, but also to infectious and chronic inflammatory diseases. It was found that the manifestations of systemic osteoporosis include an increase in atrophic processes in the jaw bones. A decrease in the level of 1.25 (OHhD3 in postmenopausal women plays an important role in the development of osteoporosis. The activity of 1-a-hydroxylase is influenced by the level of estrogen.
In periodontitis, osteoclastic resorption of periodontal bone tissue increases, which is associated in the post-menopausal period in women with insufficient estrogen synthesis.
Among the synthetic analogs of 1.25 (OH)2D3, 1aOND3 ("Oxydevit", LLC "RPK EKHO", RF) is of the greatest importance. This form of vitamin D3 has the same spectrum of action as 1.25 (OHhD3. Its high biological activity is explained by the conversion to 1.25 (OHhD3 as a result of hydroxylation involving 25OH. 1aOHD3 has a more prolonged and "mild" effect.
The purpose of the study was to comparatively establish the effect of main active metabolites of cholecalciferol on the periodontal condition of rats under conditions of experimental estrogen deficiency and bone injury.
Materials and methods. The experiment was carried out on 31 female breeding Wistar rats. Group 1 (8 animals) consisted of intact rats. At 2 months of age, the rats of Groups 2-4 underwent ovariectomy, as well as a femoral fracture of one of the hind limbs 1 month before sacrifice. Group 2 (control) consisted of 8 rats (ovariectomy+fracture). Rats of the 3rd and 4th groups, starting from the next day at 2 months of age, were given per os preparations: the 3rd group (8 rats) - 1aOHD3 at a dose of 0.1 ^g day/rat; in Group 4, 7 rats were injected with 24,25(OH)2D3 at a dose of 1.25 ^g day/rat (LLC "RPK EKHO", RF). At the end of the experiment, the rats were sacrificed by total exsanguination from the vessels of the heart under anesthesia with thiopental (40 mg/kg). All experiments were carried out in accordance with the European Convention for the Protection of Vertebrate Animals used for Experimental or other Scientific Purposes (Strasbourg, 1986). Having previously separated the oral mucosa and submandibular salivary glands, maxilla and mandible were isolated. Resorption of the alveolar bone was assessed on freshly isolated jaws.
The objects of biochemical studies were the oral mucosa, submandibular salivary glands, alveolar bone, liver, femoral muscle, femur. The lipid peroxidation level (LPL) was assessed by the content of diene conjugates (DC) [4] and malondialdehyde (MDA). The activity of antioxidant enzymes was determined: glutathione reductase (GR) [8] and glutathione peroxidase (GPx) [12], as well as the state of the thiol-disulfide system [9]. In the liver, the content of DNA and RNA was determined [1]. The content of polyenoic fatty acids was determined in liver lipids by gas-liquid chromatography.
The experimental results were processed by conventional statistical methods with the determination of t-criteria for the reliability of differences according to Student's t-test.
Results of the study and their discussion. The study on the effect of the hormonal forms of cholecalciferol 1aOHD3 and 24,25(OH)2D3 was carried out against the background of experimental ovariectomy in combination with traumatic stress of a femoral fracture (control group).
Morphometric studies of the alveolar process bone in rats showed that the experimental pathogenic effect did not significantly change the parameters of bone resorption of the periodontal bone (table 1).
Experimental ovariectomy performed in rats in combination with a femoral fracture significantly increased the level of diene conjugates in the liver by 5.4 times (p <0.001) compared to the intact group, which indicates the intensification of LPL processes in this study object (Table 1). In the bone of the alveolar bone and in the femoral muscle, the increase in the level of the primary LPL products, diene conjugates, was not significant (3% and 52%, respectively, Table 2). In the control group, the activity of glutathione peroxidase in the liver increased by 1.5 times (p = 0.05) compared to the intact group, which
was apparently inductive in response to an increase in the amount of LPL products in this study object. In the femoral muscle, the activity of glutathione peroxidase was not significantly changed; glutathione reductase decreased by 25% (p = 0.07), which indicated insufficient functioning of glutathione metabolism enzymes in this study object (table 2).
LPL indices and the activity of glutathione metabolism enzymes were studied in the oral mucosa and submandibular salivary glands (Table 3). Thus, the MDA content in the control group is increased by 54% in comparison with the intact group (p <0.001); in the submandibular salivary glands - by 81% (p <0.001). The activity of glutathione peroxidase in the oral mucosa increased by 1.4 times (p <0.001). Glutathione reductase activity did not change significantly (table 3). The study of nucleic acids content in the liver under conditions of ovariectomy and bone injury revealed the following: the level of DNA decreased by 5.6 times (p <0.001); RNA - by 2.9 times (p <0.001; Table 4). Experimental estrogen deficiency in combination with a traumatic fracture of the femur caused significant changes in the liver of rats in its fatty acid composition. Thus, the content of arachidonic acid (20:4) significantly decreased in liver lipids (by 66%; p = 0.001): 7.81±0.62% versus 11.7±1.0% in the intact group. The level of eicosapentaenoic acid (20:5) in the control group decreased by 65% (trend; p = 0.10): 1.21±0.18% versus 1.86±0.33%. The content of docosahexaenoic acid (22:6) significantly decreased by 67% (p = 0.011): 4.61±0.25% versus 6.90±0.65% in the intact group.
Morphometric study of periodontal bone resorption showed that 1aOHD3 did not significantly affect, and 24,25 (OH)2D3 reduced the alveolar bone resorption in rats by 12% (trend; p1 = 0.08; 100% in the control group; table 1).
Table 1
The effect of vitamin D3 metabolites on the resorption parameters (%) of the alveolar bone in rats (M±m; p1)
Studied index Groups of animals
1 2 3 4
Alveolar bone resorption (%) (mean values) 43.0±1.5 43.5±1.6 42.4±1.1 38.2±2.3 P1=0.08
Notes. In table 1, the reliability index p is calculated in comparison with the control group ("ovariectomy+fracture")
Of the two studied hormonal forms of vitamin D3, 24,25 (OH)2D3 significantly reduced (p <0.001) the level of the primary LPL products - diene conjugates in the liver of rats and doubled (p1 <0.001) the activity of glutathione peroxidase, which indicates an overall positive effects on the organism of rats (table 2). The content of diene conjugates in the femoral muscle decreased to a greater extent 1aOHD3 than 24,25(OH)2D3 (Table 2). 1aOHD3 increased the activity of glutathione peroxidase by 55% (p: <0.001). 24,25 (OH)2D3 increased the activity of glutathione reductase by 17% (p1 <0.002; table 2).
Table 2
The effect of vitamin D3 metabolites on the LPL state and the activity of antioxidant enzymes in rats' tissues (M±m; p; p1)
Studied index Groups of animals
1 2 1 3 4
Content: DC (extinction units/g) liver
0.37±0.13 2.00±0.010 p<0.001 1.86±0.11 0.16±0.090 P1<0.001
Activity: GR (nmol/s.g.) 0.42±0.13 0.47±0.099 1.43±0.90 -
GPx (nmol/s.g.) 8.10±0.92 12.5±2.20 14.0±3.86 26.6±0.64 p1<0.001
femoral muscle
Content: 0.33±0.11 0.50±0.14 0.054±0.015 0.17±0.049
DC (extinction units/g) P1 = 0.006 P1 = 0.04
Activity: GR (nmol/s.g.) 3.90±0.48 2.91±0.12 p=0.07 1.25±0.23 P1 < 0.001 3.41±0.013 P1 = 0.002
GPx (nmol/s.g.) 12.6±0.83 13.3±0.46 20.6±1.012 P1 < 0.001 13.2±5.61
alveolar bone
Kinetics of MDA accumulation (%) 1st hour of incubation 114±2.7 117±4.7 124±3.8 134±99.2
2nd hour of incubation 121±2.4 129±4.2 162±55.1 145±9.3
femoral bone
Kinetics of MDA accumulation (%) 127±5.9 178±7.5 100±0.00
1st hour of incubation P1 < 0.001 P1 = 0.001
2nd hour of incubation - 147±8.2 165±0.00 P1 = 0.05 175±23.4
Notes. In tables 2-5, the reliability index p was calculated in comparison with the intact group; pi -compared to the control ("ovariectomy+fracture")
The parameters of the kinetics of MDA accumulation under the influence of the studied drugs in the femur underwent significant changes (table 2). So, if 1aOHD3 increased the kinetics of MDA accumulation during 1- and 2-hours incubation, then 24,25-dioxycholecalciferol decreased this index by 21% even after 1-hour incubation (p1 = 0.001). Hormone-active forms of cholecalciferol under these experimental conditions did not significantly change the kinetics of MDA accumulation in the alveolar bone (table 2).
Table 3
The effect of vitamin D3 metabolites on the LPL state and the activity of antioxidant enzymes in rats' oral tissues (M±m; p; p1)
Groups of animals
Studied indices 1 2 3 4
oral mucosa
Content: MDA (^mol/g) 0.041±0.0010 0.063±0.0056 p=0.001 0.035±0.0075 pi = 0.011 0.033±0.0075 p1 = 0.008
Activity: GR (nmol/s.g.) 3.40±0.098 3.37±0.096 1.76±0.037 P1 < 0.001 3.03±0.25
GPx (nmol/s.g.) 12.9±0.38 17.5±2.06 p=0.04 23.6±1.32 p1 = 0.02 -
submandibular salivary glands
Content: MDA (^mol/g) 0.054±0.005 0.098±0.0038 p < 0.001 0.096±0.0052 0.10±0.018
Activity: GR (nmol/s.g.) 0.61±0.097 0.67±0.054 0.21±0.046 P1 < 0.001 1.01±0.085 p1 = 0.005
GPx (nmol/s.g.) 16.4±0.89 23.2±1.03 p < 0.001 27.8±0.79 p1 = 0.004 31.1±1.01 P1 < 0.001
We studied the changes in LPL indices and the activity of glutathione metabolism enzymes were studied in the oral mucosa and submandibular salivary glands (table 3). The content of MDA under the influence of 1aOHD3 and 24.25 (OH)2D3 decreased in the oral mucosa by 1.8 and 1.9 times (p1 = 0.008), respectively. Both metabolites did not significantly change the studied parameter in the submandibular salivary glands in comparison with the data of the control groups (table 3). 1aOHD3 increased by 35% (p1 = 0.02) glutathione peroxidase activity in the oral mucosa and by 14% (p1 = 0.004) in the submandibular salivary glands and significantly reduced the activity of glutathione reductase in submandibular salivary glands as compared to the control groups. 24.25(OH)2D3 significantly increased the activity of both glutathione metabolism enzymes in the submandibular salivary glands (table 3).
Under the influence of 1aOHD3, the DNA content in the liver increased by 2.9 times (pi=0.02; table 4). The RNA level increased by 3.4 times (p1<0.001) under the influence of 1aOHD3 and 24.25(OH)2D3 compared to the control groups (table 4).
Table 4
The effect of vitamin D3 metabolites on the content of RNA and DNA in the liver of rats (M±m; p; p1)
Studied indices Groups of animals
1 2 3 4
Content (mcg/g): DNA 151±9.90 27.1±16.0 p<0.001 79.8±11.5 p1 = 0.02 54.2±11.5
RNA 151±4.30 52.1±8.70 p<0.001 179±19.5 P1<0.001 175±20.1 P1<0.001
The study of the fatty acid composition of liver lipids under the influence of preparations of hormonal forms of cholecalciferol revealed the following. Thus, 1aOHD3 increased the arachidonic acid content(20:4) by 36% (p1=0.08):10.6±1.3% vs. 7.81±0.62%; 24,25 (OH^ - by 33% (p1 = 0.05): 10.4±1.0% vs. 7.81±0.62% compared to the control groups. This active metabolite significantly increased the level of oleic acid (18:2) by 19% (p1 = 0.04): 27.0±1.6% versus 22.7±0.9% and docosahexaenoic acid (22:6) by 25%: 5.75±0.53% versus 4.61±0.25% (trend; p1 = 0.08).
Under the influence of risk factors for the periodontitis development (aging and chronic traumatic stress), the protective properties of hormonally active metabolites of vitamin D3 were observed. They were expressed in the inhibition of LPL processes in the oral mucosa of rats, as well as periodontal protective effects when testing 24.25-dihydroxy vitamin D3.
In the course of the studies, it was found that under the influence of risk factors for periodontitis (aging and chronic traumatic stress), LPL processes were activated both at the level of the body - in the liver, and in the tissues of the oral cavity - in the oral mucosa and submandibular salivary glands. The high biological activity of peroxidation products in biomolecules necessitates the constant functioning of a
special mechanism of antioxidant system in the cells, the most important components of which are antioxidant enzymes [3, 14].
The increase in glutathione peroxidase activity in the liver, oral mucosa and submandibular salivary glands was compensatory in response to the activation of peroxide processes in these study objects. An excess of peroxides can contribute to the oxidative destruction of not only lipids, but also proteins. It is generally accepted that the oxidative modification of proteins plays a key role in the molecular mechanisms of oxidative stress and may be a trigger for damage to other biomolecules (DNA and RNA) of the cell. Thus, in our studies, ovariectomy with bone injury caused a significant decrease in the levels of RNA and DNA in liver cells, as well as changes in the fatty acid composition of its lipids, apparently as a result of peroxide destruction.
In our experiments, hormonal forms of vitamin D3 - 1aOHD3 and 24.25 (OH)2D3 were used in conditions of ovariectomy and chronic bone injury. The protective properties of the two hormonal forms were expressed in the inhibition of LPL processes in the oral mucosa, as well as in the activity of glutathione metabolism enzymes - glutathione reductase and glutathione peroxidase in the submandibular salivary glands. Both hormonal forms of vitamin D3 increased the level of RNA, and 1aOHD3 increased the DNA content in the liver. 24.25(OH)2D3 significantly reduced the level of LPL processes in the liver and activated glutathione peroxidase, which provides protection against the damaging effects of peroxides of different nature. A decrease in resorptive processes in the periodontal bone tissue caused 24.25 (OH)2D3; in the femur - a significant decrease in LPL processes.
Insufficient anti-resorptive effect of 1a-dihydroxyvitamin D3, as well as an increase in MDA level in the femur (in case of its fracture), on the one hand, are associated with a significant pathogenic effect, as well as the fact that metabolizing, 1aOHD3 is converted into calcitriol gradually. At the same time, the biological activity of 1a-dihydroxyvitamin D3 in rats and humans is only half the activity of the hormonal form of 1,25-dioxy-vitamin D3. In the liver, some leveling of the consequences of the peroxidation syndrome was observed, in particular, a partial restoration of the fatty acid composition of liver lipids when using 1aOHD3 and, to a greater extent, under the influence of 24,25 (OH)2D3. Thus, the most pronounced antioxidant properties in selected experimental conditions at the level of the rats' organism and in the tissues of the oral cavity were shown by 24.25-dioxy-vitamin D3.
The data obtained confirm the presence of antioxidant activity inherent in the vitamin D3 molecule itself [2]. It is assumed that cholecalciferol can act as a membrane antioxidant, stabilizing membranes and protecting them from LPL through interaction with their hydrophobic regions [6, 11]. According to the literature, calcitriol (1.25 (OH)2D3) can enhance the elimination of reactive oxygen and nitrogen forms, increasing the intracellular pool of reduced glutathione. In addition, the effects of vitamin D3 may be mediated by its anti-inflammatory activity through gene transcription of numerous anti-inflammatory cytokines [12, 13].
1. Under conditions of ovariectomy reproduction and bone trauma LPL processes in the liver, oral mucosa and submandibular salivary glands were intensified; the levels of DNA and RNA in the liver decreased, as well as the content of arachidonic acid as a result of its peroxide destruction.
2. Hormone-active metabolites of vitamin D3 under the influence of risk factors for periodontitis showed an antioxidant effect, and to a greater extent the metabolite 24,25-dioxycholecalciferol.
3. 24,25(OH)2D3 inhibited LPL processes in the liver, femur and oral mucosa; in the submandibular salivary glands it increased the activity of glutathione peroxidase; in the liver it restored RNA, as well as the fatty acid composition of its lipids. 24,25(OH)2D3 showed a periodontal protective effect.
References
1. Kutsenko LO. Riven peroksydatsiyi, vmist nukleyinovyh kyslot v tkanynah sertsia tvaryn pid vplyvom peptydiv mozku v umovah gostrogo stresu. Problemy ekolohiyi i medytsyny 2011; 15:5-6. [in Ukrainian]
2. Laricheva OM. Protsesy vilnoradykalnoho perekysnogo okysnennya ta stan antyoksydantnoho zahystu legen shchuriv iz znyzhenoyu aktyvnistyu epifizu. Visnyk problem biolohiyi i medytsyny 2015; 1: 110-114. [in Ukrainian]
3.Safonova OA, Popova TN, Saidi LA. Funktsionirovanie glutationperoksidaznoy /glutationreduktaznoy sistemy v tkanyakh krys pri deystvii tsitrata na fone razvitiya tireotoksikoza. Vestnik Voronezhskogo gosudarstvennogo universiteta. Seriya: Himiya. Biologiya. Farmatsiya. 2011; (1): 144-148. [in Russian]
4. Shyder I, Yuskiv I. Sezonnyye izmeneniya aktivnosti fermentov antioksidantnoy sistemy i produktov perekisnogo okisleniya lipidov u krolikov raznogo vozrasta, spontanno bolnykh psoroptozom. Tvarynnytstvo Ukrainy 2015; 4: 32-35. [in Russian]
5. Spirichev VB. O biologicheskikh effektakh vitamina D. Pediatriya. Zhurnal im. GN Speranskogo. 2011; 90(6): 113-119. [in Russian]
6. Christakos S. Vitamin D and intestinal calcium absorption. Molecular and cellular endocrinology. 2011; 347(1-2): 25-29. https://dx.doi.org/10.1016%2Fj.mce.2011.05.038
7. Giera S, Braeuning A. Wnt/p-catenin signaling activates and determines hepatic zonal ex.pression of glutathione S-transferases in mouse liver. Toxicological Sciences. 2010; 115(1): 22-33. https://doi.org/10.1093/toxsci/kfq033
8. Han YP. Vitamin D in liver diseases: from mechanisms to clinical trials. Journal of gastroenterology and hepatology. 2013; 28: 49-55. https://doi.org/10.1111/jgh.12016
9. Hormozi-Nezhad MR, Seyedhosseini E, Robatjazi H. Spectrophotometric determination of glutathione and cysteine based on aggregation of colloidal gold nanoparticles. Sci Iran. 2012; 19 (3):958-963. https://doi.org/10.1016/j.scient.2012.04.018
10. Kamen, DL, Tangpricha V. Vitamin D and molecular actions on the immune system: modulation of innate and autoimmunity. Journal of molecular medicine. 2010, 88(5): 441-450. https://dx.doi.org /10.1007%2Fs00109-010-0590-9
11. Kim HA, Perrelli A, Vitamin D deficiency and the risk of cerebrovascular disease. Antioxidants 2020; 9(4): 327-333. https://dx.doi.org/10.3390%2Fantiox9040327
12. Li H, Xie H. et al. 25-hydroxyvitamin D3 ameliorates periodontitis by modulating the expression of inflammation-associated factors in diabetic mice. Steroids .2013; 78(2): 115-120. https://doi.org /10.1016/j.steroids.2012.10.015
13. Luong KV, Nguyen LT. The role of vitamin D in autoimmune hepatitis. Journal of clinical medicine research 2013; 5(6):407-412. https://doi.org/10.4021/jocmr1505w
14. Spahis S, Delvin E. Oxidative stress as a critical factor in nonalcoholic fatty liver disease pathogenesis. Antioxidants & redox signaling, 2017, 26.10: 519-541. https://doi.org/10.1089 /ars.2016.6776
iV(|k-|>;iiii
ВПЛИВ ГОРМОНАЛЬНО-АКТИВНИХ МЕТАБОЛ1Т1В ХОЛЕКАЛЬЦИФЕРОЛУ НА СТАН ТКАНИН РОТОВО1 ПОРОЖНИНИ ЩУР1В В УМОВАХ ЕСТРОГЕННО1 НЕДОСТАТНОСТ1 I ТРАВМАТИЧНОГО СТРЕСУ
Шнайдер С.А., Гуменюк В.В., TopoxiBCbKm В.Н., Ефремова О.В., Христова М.Т., Ткаченко Е.К.
Метою дослщження було порiвняльне вивчення впливу активних метаболтв втмшу D3 на стан пародонту щурiв в умовах експериментально! естрогенно! недостатност та травматичного стресу. Дослщження проведено на 31 щур^самщ лшп Вютар стадного розведення. 1-я група - штактна (8 особин). Щурам 2-й - 4-о! груп була проведена оварiектомiя i перелом стегново! истки. 2-я група - контрольна (8 щурiв); щури 3-й - 4-о! груп на rai проведеного патогенного впливу отримували препарати per os: 3-! групи (8 щурiв) - 1aOHD3 в дозi 0,1 мкг в день на щура; в 4-й грут (7 щурiв) - 24,25 (ОН) 2D3 в дозi 1,25 мкг в день/щура. На момент виведення з експерименту тварини знаходилися у вщ 15 мюящв. В умовах впливу факторiв ризику пародонтиту спостерталися захисш властивост гормонально-активних метаболтв втмшу D3, що виразилися в гальмуванш процеЫв перекисного окислення лтвдв у слизовш оболонщ порожнини рота щурiв, а також пародонтопротекторна ефекти при застосуванш 24,25-дюкЫвтмша D3.
Ключовi слова: метаболии втмшу D3, естрогенна недостатшсть, травматичний стрес, пародонтопротекторш властивоси, антиоксидантна дiя, щури.
Стаття надшшла 18.08.2019 р.
ВЛИЯНИЕ ГОРМОНАЛЬНО-АКТИВНЫХ МЕТАБОЛИТОВ ХОЛЕКАЛЬЦИФЕРОЛА НА СОСТОЯНИЕ ТКАНЕЙ РОТОВОЙ ПОЛОСТИ
КРЫС В УСЛОВИЯХ ЭСТРОГЕННОЙ НЕДОСТАТОЧНОСТИ И ТРАВМАТИЧЕСКОГО СТРЕССА
Шнайдер С.А., Гуменюк В.В., Горохивский В.Н., Ефремова О.В., Христова М.Т.,Ткаченко Е.К.
Целью исследования явилось сравнительное изучение влияния активных метаболитов витамина D3 на состояние пародонта крыс в условиях экспериментальной эстрогенной недостаточности и травматического стресса. Опыт проведен на 31 крысе-самке линии Вистар стадного разведения. 1-я группа - интактная (8 особей). Крысам 2-й - 4-ой групп были проведены овариэктомия и перелом бедренной кости. 2-я группа - контрольная (8 крыс); крысы 3-й - 4-ой групп, на фоне проведенного патогенного воздействия, получали препараты per os: 3-й группы (8 крыс) - 1aOHD3 в дозе 0,1 мкг в день на крысу; в 4-й группе (7 крыс) - 24,25(OH)2D3 в дозе 1,25 мкг в день/крысу. На момент выведения из эксперимента животные находились в возрасте 15 месяцев. В условиях воздействия факторов риска пародонтита наблюдались защитные свойства гормонально-активных метаболитов витамина D3, выразившиеся в торможении процессов перекисного окисления липидов в слизистой оболочке полости рта крыс, а также пародонтопротекторные эффекты при применении 24,25-диоксивитамина D3.
Ключевые слова: метаболиты витамина D3, эстрогенная недостаточность, травматический стресс, пародонтопротекторные свойства, антиоксидантное действие, крысы.
Рецензент Срошенко Г. А.
