Background: Although isotretinoin has been confirmed by clinical and experimental studies to be a teratogenic agent that causes fetal developmental abnormalities, its effects on placental development and placental-like extra-embryonic vascularization have not been sufficiently studied. The vascularization of the chorioallantoic membrane is structurally and functionally similar to mammalian placental vascularization, which provided the rationale for conducting this study. Aim: To study the effect of isotretinoin on chorioallantoic membrane vascularization using an in ovo chick embryo model. Materials and Methods: A comparative experimental control study was conducted using fertilized eggs of the same developmental age from Gallus gallus domesticus. At the HH10 embryonic stage, the control group received avian saline, while the experimental group was administered isotretinoin (5 µg/100 µL). Vascularization of the yolk sac and chorioallantoic membrane was evaluated at the macro- and tissue levels at 72 and 120 hours of embryonic development. Vessel branching order, vascular density, and capillary number were compared, and statistical analysis was performed using the Mann-Whitney U test. Result: In the control group, vascularization progressed actively, with abundant formation of third and fourth order vessels, resulting in a dense reticular network. In contrast, the isotretinoin treated group showed delayed vessel branching, a marked reduction in the number of third- and fourth-order vessels, and an overall decrease in vascular density of 40–60%. Histological analysis revealed thinning of the chorioallantoic membrane, loss of tissue layers, and thinning of vascular walls, and the number of capillaries was significantly lower than in the control group (p<0.01). In addition, the development of chorioallantoic membrane vascularization in chick embryos was found to be structurally and developmentally similar to mammalian placental vascularization. Conclusion Isotretinoin was shown to inhibit the development of the chorioallantoic membrane and markedly reduce vascularization and differentiation in an in ovo chick embryo model.

Background: Dysregulation of inflammation underpins chronic cardiovascular, metabolic, neurodegenerative, and neoplastic conditions. Traditional medicine has long utilized medicinal plants to alleviate and treat systemic inflammation. Specifically, Rhodiola rosea L. and Rhodiola quadrifida (Pall.) Fisch. & C.A.Mey. possess anti-inflammatory, antitumor, antioxidant, and anti-angiogenic properties. Saposhnikovia divaricata (Turcz.) Schischk. has been shown to exert anti-inflammatory effects, support musculoskeletal function, and enhance tissue regeneration. Furthermore, Salsola laricifolia Litv. has been studied for its antioxidant, immunomodulatory, and anti-inflammatory activities. Although the individual anti-inflammatory, antioxidant, and antitumor activities of these plants are established, research evaluating the combined effect of their combined extract remains scarce, providing the rationale for this study. Aim: To evaluate the in vitro effects of a combined extract derived from these medicinal plants on the expression of selected pro-inflammatory cytokines. Materials and Methods: A dry combined extract consisting of Rhodiola rosea, Rhodiola quadrifida, Salsola laricifolia, and Saposhnikovia divaricata was prepared at the Chemistry and Technology Sector of the Institute of Pharmaceutical Research, Monos Group. An in vitro inflammation model was established using murine RAW264.7 macrophage-like cells stimulated with lipopolysaccharide (LPS, 100 ng/mL). Cell viability was assessed using the CCK-8 assay, while the output of pro-inflammatory cytokines TNF-α and IL-6 was measured via Enzyme-Linked Immunosorbent Assay (ELISA). Statistical analysis was performed using one-way ANOVA. Result: The combined plant extract demonstrated no cytotoxic effects on RAW264.7 cells across the tested concentration range. In LPS-stimulated RAW264.7 macrophages, the composite extract dose-dependently and significantly suppressed the production of the pro-inflammatory cytokines TNF-α (p<0.001) and IL-6 (p<0.0001). Conclusion 1. The combined extract of Saposhnikovia divaricata, Rhodiola rosea, Rhodiola quadrifida, and Salsola laricifolia exhibited no cytotoxicity in vitro within the range of 50–400 µg/mL. 2. The combined herbal extract significantly suppressed the production of pro-inflammatory cytokines TNF-α (p<0.01) and IL-6 (p<0.001) in LPS-induced RAW264.7 macrophages in a concentration-dependent manner.

Background: In recent years, natural compounds have been shown to play an important role in cancer prevention and early-stage therapy. Flavanones, a class of polyphenolic compounds present in plants, vegetables, seeds, fruit peels, and flowers, have been identified to possess anticancer, antioxidant, anti-inflammatory, and antibacterial bioactivities. Cancer has become a major global economic and public health challenge. According to international statistics, one in four individuals (22.8%) die from non-communicable diseases, while one in six (16.8%) die from cancer. Aim: To investigate the effect of a flavanone (5,2’,3’-trihydroxy-6,7-methylenedioxyflavanone) isolated from Iris tenuifolia on the migration of liver cancer cells. Materials and Methods: The study was conducted at the Institute of Biomedicine, Mongolian National University of Medical Sciences. The effect of the flavanone (5,2’,3’-trihydroxy-6,7-methylenedioxyflavanone) on cancer cell migration was evaluated in vitro using the scratch assay. Human liver cancer cells (HepG2) were revived and stabilized before experiments were performed. Results: HepG2 cells were treated with a 2.5 μg/mL concentration of the flavanone for 24 hours. In the control group, an initial scratch width of 0.9 mm was reduced to 0.65 mm after 24 hours due to cell proliferation and migration into the denuded area. However, treatment with the 2.5 μg/mL flavanone concentration resulted in the complete inhibition of cell migration. Conclusion The flavanone isolated from Iris tenuifolia effectively suppresses the migration of liver cancer cells.

Background: In recent years, scientists have found that certain natural compounds have significant potential in cancer prevention and early-stage cancer treatment. Flavanones, a class of polyphenolic compounds found in plants, vegetables, seeds, fruit peels, and flowers, have been identified to possess anticancer, antioxidant, anti- inflammatory, and antibacterial bioactivities. Cancer has become a major global challenge in terms of both economic and public health concerns. Global statistics indicate that 22.8% of deaths are attributed to non-communicable diseases, and 16.8% are caused by cancer, accounting for one in four and one in six deaths, respectively. Aim : To investigate anticancer effects of Iris Tenuifolia-derived flavanone on cancer cell lines. Materials and Methods : The study was conducted at the Bio-Medical Research Institute of the Mongolian National Uni versity of Medical Sciences, investigating the effect of flavanones on cancer cell viability under in vitro conditions using the MTT assay. In the study, colon, liver, and lung cancer cells were cultured, stabilized, and used for the experiments. Colorectal cancer cells (MC38), liver cancer cells (HepG2), and lung cancer cells (A549) were revived, cultured, and stabilized for use in the experimental procedures. Statistical analysis of the results was performed using Microsoft Excel 2010, and graphs were generated using GraphPad Prism 8. Differences between groups were analyzed using Student’s t-test, and a p-value of <0.05 was considered statistically significant. Results : We treated MC38, HepG2, and A549 cancer cells with different concentrations of flavanone (2.5 µM, 5 µM, and 10 µM) for 24 to 48 hours to evaluate cell viability. Flavanone inhibited A549 cell viability by 2.5 μM-10%, 5 μM-25%, and 10 μM-38%, respectively. For HepG2 cells, flavanone treatment at concentrations of 5-10 µM reduced cell viability by 28–58%. No statistically significant effect on the viability of MC38 cells was observed following treatment with flavanone at concentrations ranging from 2.5 to 10 µM. Additionally, although MC38 inhibited cell viability in a dose-de pendent manner in cell cultures, it had a statistically significant effect at higher concentrations of 30-200 μM (p<0.01). Conclusion Flavanone inhibits the cancer cell viability in a dose and time dependent manner

Background: The study of small-molecule compounds with antitumor activity involves several crucial steps. These include determining their selective effects on cancer cells, understanding the type of cell death they induce, identifying the activated signaling pathways, pinpointing the target molecules, and elucidating the mechanisms of action. Among the plant-derived compounds with anticancer properties, flavonoids are notable for their ease of isolation and their abundance in food. Apigetrin, a representative flavonoid, is a secondary metabolite found in plants, and our previous study indicated that its anticancer selectivity index was 13.1. However, the specific mechanism by which apigetrin inhibits leukemia cell growth remains unclear. Aim: To study of the inhibitory action of apigenin on leukemia cell culture Materials and Methods: In this study, we evaluated the apoptosis of cells using flow cytometry and investigated the in volvement of the caspase pathway through the use of pancaspase inhibitors to explore the effects of apigetrin on leukemia cell growth. Results: After incubating leukemia RAW264.7 cells with 30 μM apigetrin for 24 and 48 hours, we did not detect any apoptosis through Annexin V and PI staining by flow cytometry. We compared the number of viable cells using the MTT assay after 24-hour treatment of apigetrin with or without pretreatment of Z-VAD, a pancaspase inhibitor, for 30 minutes. The results indicated that the pancaspase inhibitor did not reduce the inhibitory effect of apigetrin on the growth of RAW264.7 cells. In contrast, the positive control group, treated with doxorubicin—which induces apoptosis—showed not only significant apoptosis but also a reduction of the pancaspase inhibitor on the cell growth inhibition. Therefore, these data suggested that apigetrin likely has a cytostatic effect or inhibits the cell cycle rather than being cytotoxic. Future research should focus on determining which stage of the cell cycle RAW264.7 cells treated with apigetrin are in, as well as studying the signaling pathways involved in the cell cycle. Conclusions Apigetrin inhibits the proliferation of RAW264.7 leukemia cells in a caspase-independent and non-apoptotic manner.

Background: Cervical cancer is a common disease among women. Treatment for cervical cancer includes surgery, radiation therapy, chemotherapy, or a combination of chemotherapy and radiation therapy. Cisplatin is the first-line chemotherapy drug for cervical cancer. Research has shown that about 20% of cervical cancer patients become resistant to chemotherapy, which results in decreased results, tumor recurrence, and poor prognosis. Therefore, researching new drugs, improving the sensitivity of cervical cancer cells to cisplatin, and improving the effectiveness of cervical cancer treatment is the basis of this research. Aim: To investigate the inhibitory effect of curcumin on cisplatin-resistant cervical cancer Hela/DDP and SiHa/DDP cell lines. Materials and Methods: The study utilized cisplatin-resistant cervical squamous carcinoma (SiHa/DDP) and adenocarcinoma (Hela/DDP) cell lines. The cells in the experimental group were treated with 8.5 μM of curcumin, while the control group received only the culture medium. A colony formation assay was conducted to assess cell proliferation, with colonies stained using crystal violet; the number of colonies was then counted and compared between the two groups. Results : 1. In the Hela/DDP cell line, the control group formed an average of 507.7±15.70 colonies, whereas the experimental group, treated with curcumin, formed 112.3±16.17 colonies. The difference between the groups was statistically significant (p < 0.0001). 2. In the SiHa/DDP cell line, the control group had an average of 450.3±17.95 colonies, while the experimental group treated with curcumin had 198.3±13.05 colonies. This difference was also statistically significant (p < 0.0001). Conclusions 1. Curcumin significantly reduces the proliferation of cisplatin-resistant cervical squamous cell carcinoma (Hela/DDP) cells. 2. Curcumin significantly reduces the proliferation of cisplatin-resistant cervical adenocarcinoma (SiHa/DDP) cells.

Background: Rhododendron adamsii (Sagaan Dalya) is a medical plant widely distributed in the Altai region, Mongolia, and Russia. It is traditionally used for its calming, restorative, and immune-boosting properties. Inflammation is a complex immune response against pathogens such as bacteria, viruses, and fungi, involving macrophages, fibroblasts, mast cells, and neutrophils. These cells release inflammatory mediators such as nitric oxide (NO), TNF-α, and IL-1β. In collaboration with the Russian Foundation for Basic Research, a project was initiated to investigate the bioactive fractions of Rh. rosea (L.) and Rh. adamsii and their effects on the production of TLR4 signaling end products and associated protein activation. Previous studies within this project have shown that certain bioactive fractions exhibit anti-inflammatory activity. Specifically, fraction 7.11 suppressed NO production and inflammatory signaling molecules in LPS-stimulated RAW 264.7 macrophages, while fractions 7.46 and 7.52 influenced the phosphorylation of proteins such as ERK1/2, JNK, and IRF3. These findings suggest the need for further investigation into the effects of Rh. adamsii bioactive fractions on inflammatory signaling pathways. Aim: This study aims to evaluate the effects of bioactive fractions derived from Rhododendron adamsii on the production of TLR4 signaling end products in RAW264.7 macrophage cell cultures. Materials and Methods: The study was conducted using RAW264.7 macrophage cell cultures and bioactive fractions extracted from Rh. adamsii, dividing the experiments into three groups. After stabilization, RAW264.7 cells were stimulated with 100 ng/mL LPS. Based on previous studies, non-toxic concentrations of bioactive fractions (10 µg/mL) were applied. NO production was measured using the Griess assay, while TNF-α and IFN-β cytokine levels were evaluated using ELISA. Each experiment were repeated three times, and data were statistically analyzed using SPSS 25.0, applying One-way ANOVA and Independent Samples T-test. Results: The NO production in the positive control group was significantly higher compared to the negative control. In contrast, the experimental groups showed a statistically significant reduction in NO production, suggesting a potential inhibitory effect on TLR4 signaling in macrophages. However, fraction 7.48 reduced TNF-α levels while increasing IFN-β production, but these changes were not statistically significant. Similarly, fraction 7.55 slightly reduced TNF-α and IFN-β levels, but the effect was also statistically unsignificant. Conclusion The bioactive fractions 7.48 and 7.55 of Rh. Adamsii reduced nitric oxide (NO) production in LPS-stimulated macrophage cell line cultures, suggesting that they may inhibit TLR4 signaling. However, their lack of effect on TNF-α and IFN-β production indicates that they do not influence TLR4 signaling mediated by these cytokines. Instead, they may affect the final product output through other pathways or different stages of signal transduction.

Background: In recent years, natural compounds have been shown to play an important role in cancer prevention and early-stage therapy. Flavanones, a class of polyphenolic compounds present in plants, vegetables, seeds, fruit peels, and flowers, have been identified to possess anticancer, antioxidant, anti-inflammatory, and antibacterial bioactivities. Cancer has become a major global economic and public health challenge. According to international statistics, one in four individuals (22.8%) die from non-communicable diseases, while one in six (16.8%) die from cancer. Aim: To investigate the effect of flavanone (5,2’,3’-trihydroxy-6,7-methylenedioxyflavanone) isolated from Iris tenuifolia on the migration of lung cancer cells. Materials and Methods: The study was conducted at the Institute of Biomedicine, MNUMS. The effect of flavanone (5,2’,3’-trihydroxy-6,7-methylenedioxyflavanone) on cancer cell migration was evaluated in vitro using the scratch assay. Human lung cancer cells (A549) were revived and stabilized before experiments were performed. Results: We treated A549 cancer cells with different concentrations of flavanone (1.25 μg/ml, 2.5 μg/ml) for 24 hours and analyzed them using the scratch assay. A cell-free gap of 0.9 mm in width was created, and after 24 hours, A549 cells migrated and proliferated into the gap, reducing its width to 0.25 mm. Treatment with 2.5 μg/ml flavanone completely inhibited cell migration. Conclusion Flavanone isolated from Iris tenuifolia inhibits lung cancer cell migration in a doseand time-dependent manner.

Background: Studying the human embryonic and fetal organ systems development patterns and determining their quantitative indicators is of scientific and practical importance in medicine and health in every nation.
Distortions and pathologies during the development of the embryo are the causes of congenital disabilities. Among the congenital malformations, facial malformations are the 3rd place, including cleft lip and palate in 70% and Srouzon's syndrome in 30%. In addition, abnormalities due to changes in the size, shape, and position of the jaw are also mentioned in the 2021.04.21 issue of Morphology magazine in the study "Morphometric parameters of the bones of the skull and face during the development of newborns and fetuses". In our country, Ariuntuul G (2005) determined that cleft lip and cleft palate occur at 0.76/1000 or 1 in 1314 live births, while Ayanga G (2012) found that it occurs at 1 in 1072 live births or 0.93/1000. Moreover, the eye cup dimensions of Mongolian fetuses aged 16 36 weeks have a positive linear relationship with the gestational age determined using ultrasound by Nandintsetseg B (2015) et al. Compared with the other countries, the eyecup is slightly wider, and the outer edge distance is similar, whereas the inner edge distance is shorter. Purpose: To summarize research work and determine the embryonic development of bones involved in the formation of the face and facial parts, the period of bone formation, the point of ossification, and the period of formation. Methods: During fetal development, human organ systems grow and develop at different rates but in a particular relationship. This feature of growth and development is also clearly observed in the structure of the head and facial bones, and the results of researchers who have studied this aspect are selected in the articles. Results: Embryonic and fetal development of bone are clinically significant not only from the point of view of its morphogenesis but also from the point of view of congenital disabilities. Conclusion In the analysis of the sources, most of the works on the prenatal period of the development of the same body have studied the development of specific structures of the face and facial area, such as the palatine bones and nasal bones, or have generally covered the development of particular systems in the embryo and fetus, and face, there are relatively few works that show the entire dynamics of growth and development of facial bones.

BACKGROUND. Prostaglandin E2 (PGE2) is the most abundant prostanoid and a very potent lipid mediator, and is produced predominantly from arachidonic acid by it’s tightly regulated cyclooxygenases (COXs) and prostaglandin E synthases. PGE2 is involved in regulating many different fundamental biological functions, including immune responses. Recently, we have demonstrated that bacterial LPS induces NO production in auditory cells via an inducible NO synthase expression. The LPS-induced production of an excessive NO amount is suggested to cause injury of auditory cells, followed by ototoxicity. Auditory cells injured by such an inflammatory response must be accompanied by tissue repair and remodeling. In order to clarify the production of PGE2 in auditory cells for regulation of inflammatory response or tissue repair AIM: We aimed to examine an effect of LPS on the production of prostaglandin E2 in auditory cells. MATERIALS AND METHODS: The murine auditory cell line HEI-OC1 was established from long-term cultures of immortomouse cochlea and used as conditionally-immortalized auditory cells. HEI-OC1 cells were stimulated with or without LPS. The concentration of PGE2, TNF-α, IL-1β in the culture supernatant was determined with ELISA. COX-2 protein expression and mRNA were measured by immunoblotting and reverse transcription PCR, respectively. The bands were quantified by densitometric analysis using ImageJ software. Statistical analysis was performed using Student’s t-test and P values < 0.05 were considered significant. All experiments were performed independently at least three times. Data represent the mean value of triplicates SD. RESULT: HEI-OC1 auditory cells constitutively produce a small amount of PGE2. LPS augmented the PGE2 production via enhanced cyclooxygenase 2 (COX2) expression. LPS-induced augmentation of COX2 expression was dependent on up-regulation of COX2 mRNA expression. LPS induced the production of TNF-a, but not IL-1b An anti-TNF-α neutralizing Ab significantly inhibited PGE2 production and COX2 mRNA expression in response to LPS. LPS-induced PGE2 production was prevented by a series of pharmacological signaling inhibitors to NF- κB and MAPKs. Pam3CSK4 as a TLR2 ligand, as well as LPS as a TLR4 ligand, augmented the PGE2 production. However, poly I:C as a TLR3 ligand, imiquimod as a TLR7 ligand and CpG DNA as a TLR9 ligand did not augment it. HEI-OC1 cells expressed TLR2, TLR4 and TLR9, but not TLR3 or TLR7. CONCLUSION: The auditory cells produce PGE2 in response to LPS via COX2 expression. The PGE2 production may be involved in tissue repair and remodeling in the organ of Corti. Auditory cells might be important effector cells in host response to infection and inflammation in the organ of Corti and cochleae.