7 research outputs found
The effect of perioperative analgesia with omnopon and parecoxib on the endocytic activity of murine phagocytes on the model of tumor surgery
We used the model of surgical tumor removal to compare the effect of anesthesia with opioid analgesic omnopon and selective cyclooxygenase-2 inhibitor parecoxib on the endocytic activity of phagocytes of different localization sites. 50 C57/black mice were transplanted with Lewis lung carcinoma in the hind paw pad. After 22 days, the tumor paw was amputated. Analgesics (omnopon 10 mg/kg, parecoxib β 20 mg/kg) were administered 30 min before the operation and once per day for 3 days after the surgery. Assessment of the endocytic activity of phagocytes was performed by FACS analysis before the surgery, at days 1 and 3 after the surgery. It was found that parecoxib analgesia maintained the endocytic activity of blood and spleen phagocytes in the postoperative period. At day 3 after the surgery in parecoxib-treated animals phagocytic activity of splenic granulocytes were 2.2 times higher compared to that in the group receiving opioid analgesia. Phagocytic indices of monocytes in parecoxib-treated mice were also 1.6 and 2.5 times higher for blood and spleen monocytes, respectively. Thus, parecoxib analgesia maintained the activity of blood and spleen phagocytes in mice after the surgical tumor removal at a much higher level as compared with the omnopon analgesia
Involvement of human beta-defensin-2 in regulation of malignant potential of cultured human melanoma cells
Background and Aim: Human beta-defensin-2 (hBD-2) is an antimicrobial cationic peptide capable to control human carcinoma cell growth via cell cycle regulation. The present study was aimed on determination of hBD-2 influence on the growth patterns and malignant potential of cultured human melanoma cells. Methods: The study was performed on cultured human melanoma cells of mel Z and mel Is lines treated with recombinant hBD-2 (rec-hBD-2); cell viability, proliferation, cell cycle distribution, and anchorage-independent growth were analyzed using MTT test, direct cell counting, flow cytometry, and colony forming assay respectively. Expression and/or phosphorylation levels of proteins involved in cell cycle control were evaluated by Western blotting. Results: The treatment of mel Z and mel Is cells with rec-hBD-2 in a concentration range of 100β1000 nM resulted in a concentration-dependent suppression of cell proliferation, viability, and colony forming activity. It has been shown that rec-hBD-2 exerts its growth suppression effects via significant downregulation of B-Raf expression, activation of pRB and upregulation of p21WAF1 expression, downregulation of cyclin D1 and cyclin E resulting in cell cycle arrest at G1/S checkpoint. Conclusion: According to obtained results, hBD-2 exerts its growth suppression effect toward human melanoma cells via downregulation of B-Raf, cyclin D1 and cyclin E expression, upregulation of p21WAF1 expression and activation of pRB. Key Words: human beta-defensin-2, melanoma, proliferation, viability, cell cycle, B-Raf, anchorage-independent growth
Significance of miR-885-5p in neuroblastoma outcome
Neuroblastoma is the most common extracranial malignant solid tumor in children. This disease displays a remarkable heterogeneity in clinical behavior, ranging from spontaneous regression to rapid progression and resistance to therapy. Recent evidence has shown that microRNAs are often involved in regulation of tumor development and progression. MiR-885-5p has a tumor suppressive role in neuroblastoma, interfeΒring with cell cycle progression and cell survival. MiR-885-5p leads to the accumulation of p53 protein and activates p53-mediated pathway of cell cycle arrest, resulting in upregulation of its targets. We have analyzed association of miR-885-5p expression in 58 neuroblastoma tumors with different clinical characteristics and disease outcome. In tumor samples of patients with unfavorable clinical characteristics lower miR-885-5p expression levels were observed. Event-free survival analysis showed that low miR-885-5p expression was tightly associated with a significantly poorer outcome than in those with high expression of miR-885-5p. In this study, evidence is presented on miR-885-5p dysregulation in neuroblastoma. As follows, along with other clinical features, it can be used as an independent prognostic and possibly therapeutic approach for optimization of neuroblastoma treatment
Expression of miR-34 family of microRNA and clinical outcome of neuroblastoma
Neuroblastoma is one of the most common cancers in children that arises from sympathetic nervous system tissue with a high rate of incidence in Ukraine. Genetic abnormalities containing loss of chromosome 1p36 and 11q, MYCN amplification are strongly associated with poor prognosis of this disease. Despite rare TP53 mutations, p53 pathway is often inactivated in neuroblastoma, mostly by MDM2 overexpression. Members of miR-34 microRNA family are the most prevalent p53-induced miRNAs and important mediators of tumor suppression. MiR-34 microRNA family consists of three members: miR-34a is encoded by its own transcript from 1p36, whereas miR-34b and miR-34c share a common primary transcript in 11q. It is suggested that miR-34a is a suppressor of neuroblastoma tumor genesis, as it targets many oncogenes such as E2F3, BCL-2 and MYCN. In this study, we present evidence of miR-34 deregulation in neuroblastoma. A decrease of miR-34 expression was associated with unfavorable clinical and biological features of the disease. Low miR-34a expression was associated with a decrease of survival rates in groups of patients with MDM2 overexpression and MYCN not-amplified low expressed MDM2 neuroblastoma. Taking this into account, analysis of mir-34a expression can help to improve personalized therapy strategy and serve as additional marker for the stratification optimization in patients with neuroblastoma
Synergistic effect of microbe-associated molecules on human monocyte-derived dendritic cell maturation in vitro
Microbe-associated molecules (MAM) are known to exert stimulating effect on the dendritic cell (DC) maturation. The aim of this investigation was a comparative study of the effect of different MAMs, used separately and in combination, on human monocyte-derived DC maturation in vitro. Methods. The studied MAMs were represented by lipopolysaccharide (LPS) from Escherichia coli and different biopolymers from Staphylococcus aureus Wood 46. DC phenotype was analyzed by flow cytometry. Functional maturity of DC was assessed in the mixed leukocyte reaction. Results. The use of MAMs in combination has been shown to be more efficient for phenotypic and functional maturation of monocyte-derived DCs than utilizing different MAMs separately. The most potent stimulatory effect has been observed for the combination of LPS with peptidoglycan (PepG) or teichoic acid with PepG. Conclusions. Combined use of different MAMs, especially those that activate different signaling pathways (LPS-PepG and teichoic acid-PepG), results in synergistic stimulation of monocyte-derived DC maturation
Combined influence of teichoic acids from Staphylococcus aureus and heterometallik Cu/Cd ethylenediamine complex on peritoneal macrophages and tumor cells
We investigated the effects of teichoic acid (TA) from Staphylococcus aureus Wood 46 on tumor growth and metastasis of the experimental Lewis lung carcinoma (LLC) in mice. Intranasal administration of TA alone aggravated both tumor growth and metastasis, whereas combined administration of TA with a synthetic bimetallic (copper: cadmium) ethylene diamine complex PO244 resulted in pronounced antitumor and antimetastatic effects. The group of animals subjected to the combined treatment with TA and PO244 manifested the highest degree of lymphocyte infiltration into the tumor tissue, compared to the control group and those exposed to TA or PO244 alone. Moreover, the combined treatment negatively affected the adhesive properties of peritoneal macrophages in the LLC bearing mice. Co-cultivation of the isolated macrophages with primary LLC cultures revealed significant (p < 0.05) cytotoxic and cytostatic effects, detected as an increased level of apoptosis and a reduced fraction of replicating cells.ΠΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π»ΠΈ ΠΌΠΎΠ΄ΠΈΡΠΈΡΠΈΡΡΡΡΠ΅Π΅ Π²Π»ΠΈΡΠ½ΠΈΠ΅ ΡΠ΅ΠΉΡ
ΠΎΠ΅Π²ΠΎΠΉ ΠΊΠΈΡΠ»ΠΎΡΡ (Π’Π) Π½Π° ΡΠΎΡΡ ΠΈ ΠΌΠ΅ΡΠ°ΡΡΠ°Π·ΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ ΠΏΠ΅ΡΠ΅Π²ΠΈΠ²Π°Π΅ΠΌΠΎΠΉ ΠΊΠ°ΡΡΠΈΠ½ΠΎΠΌΡ Π»Π΅Π³ΠΊΠΈΡ
ΠΡΡΠΈΡ Ρ ΠΌΡΡΠ΅ΠΉ. ΠΡΡΠ²Π»Π΅Π½Π° Π³ΠΈΠΏΠ΅ΡΠ°ΠΊΡΠΈΠ²Π°ΡΠΈΡ ΡΠΎΡΡΠ° ΠΈ ΠΌΠ΅ΡΠ°ΡΡΠ°Π·ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΏΠ΅ΡΠ²ΠΈΡΠ½ΠΎΠΉ ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ ΠΏΡΠΈ ΠΈΠ½ΡΡΠ°Π½Π°Π·Π°Π»ΡΠ½ΠΎΠΌ Π²Π²Π΅Π΄Π΅Π½ΠΈΠΈ ΠΆΠΈΠ²ΠΎΡΠ½ΡΠΌ Π’Π, Π² ΡΠΎ Π²ΡΠ΅ΠΌΡ ΠΊΠ°ΠΊ ΠΏΡΠΈ ΠΊΠΎΠΌΠ±ΠΈΠ½ΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΌ Π²Π»ΠΈΡΠ½ΠΈΠΈ Ρ Π Π244 Π½Π°Π±Π»ΡΠ΄Π°Π»ΠΈ ΡΡΠΈΠ»Π΅Π½ΠΈΠ΅ ΠΏΡΠΎΡΠΈΠ²ΠΎ-ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠ³ΠΎ ΡΡΡΠ΅ΠΊΡΠ°. Π‘Π°ΠΌΡΠΉ Π²ΡΡΠΎΠΊΠΈΠΉ ΡΡΠΎΠ²Π΅Π½Ρ ΠΈΠ½ΡΠΈΠ»ΡΡΡΠ°ΡΠΈΠΈ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ Π»ΠΈΠΌΡΠΎΡΠΈΡΠ°ΠΌΠΈ Π·Π°ΡΠΈΠΊΡΠΈΡΠΎΠ²Π°Π»ΠΈ Π² Π³ΡΡΠΏΠΏΠ΅ ΠΆΠΈΠ²ΠΎΡΠ½ΡΡ
, ΠΊΠΎΡΠΎΡΡΠΌ ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΠ»ΠΈ ΠΊΠΎΠΌΠ±ΠΈΠ½ΠΈΡΠΎΠ²Π°Π½Π½ΡΡ ΡΠ΅ΡΠ°ΠΏΠΈΡ Π’Π Ρ Π Π 244. ΠΠΎΠΊΠ°Π·Π°Π½ΠΎ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ Π°Π΄Π³Π΅Π·ΠΈΠ²Π½ΡΡ
ΡΠ²ΠΎΠΉΡΡΠ² ΠΏΠ΅ΡΠΈΡΠΎΠ½Π΅Π°Π»ΡΠ½ΡΡ
ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ² ΠΏΠΎΠ΄ Π²Π»ΠΈΡΠ½ΠΈΠ΅ΠΌ Π±ΠΈΠΌΠ΅ΡΠ°Π»Π»ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΊΠΎΠΌΠΏΠ»Π΅ΠΊΡΠ°. ΠΠΎΡΠ»Π΅ ΡΠΎΠΊΡΠ»ΡΡΠΈΠ²ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ² ΠΎΡ ΠΆΠΈΠ²ΠΎΡΠ½ΡΡ
, ΠΊΠΎΡΠΎΡΡΠΌ ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΠ»ΠΈ ΠΊΠΎΠΌΠ±ΠΈΠ½ΠΈΡΠΎΠ²Π°Π½Π½ΡΡ ΡΠ΅ΡΠ°ΠΏΠΈΡ Ρ ΠΏΠ΅ΡΠ²ΠΈΡΠ½ΠΎΠΉ ΠΊΡΠ»ΡΡΡΡΠΎΠΉ LLC, Π²ΡΡΠ²Π»Π΅Π½ΠΎ Π·Π½Π°ΡΠΈΡΠ΅Π»ΡΠ½ΠΎΠ΅ (p < 0.05) ΡΠΈΡΠΎΡΠΎΠΊΡΠΈΡΠ΅ΡΠΊΠΎΠ΅/ΡΠΈΡΠΎΡΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΎΠ΅ Π²Π»ΠΈΡΠ½ΠΈΠ΅, ΡΡΠΎ ΠΏΡΠΎΡΠ²Π»ΡΠ»ΠΎΡΡ Π² ΡΠ²Π΅Π»ΠΈΡΠ΅Π½ΠΈΠΈ ΡΡΠΎΠ²Π½Ρ Π°ΠΏΠΎΠΏΡΠΎΠ·Π° ΠΈ ΡΠΌΠ΅Π½ΡΡΠ΅Π½ΠΈΠΈ ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΈ ΠΊΠ»Π΅ΡΠΎΠΊ ΠΏΡΠΎΠ»ΠΈΡΠ΅ΡΠ°ΡΠΈΠ²Π½ΠΎΠ³ΠΎ ΠΏΡΠ»Π°
Antineoplastic drug NSC631570 modulates functions of hypoxic macrophages
Hypoxia is an important factor in the macrophages microenvironment. Many physiological and pathological processes including solid tumor development are characterized by both low oxygen content and presence of macrophages. Tumor-associated hypoxia causes alternative polarization of macrophages in tumor tissue and transformation of these cells into the allies of a malignant neoplasm. The aim of the work was to investigate the effect of NSC631570, a cancerselective drug that is known to selectively accumulate in the tumor tissue, on hypoxic macrophage function. Murine peritoneal macrophages (PMs) were subjected to hypoxia (3% Oβ). Nitrite level was assayed by the Griess reaction. Arginase activity was measured by colorimetric method. ROS generation and phagocytosis was estimated by flow cytometry. Oββ» generation was assayed by the NBT reduction method. HMGB1 expression was determined by ELISA. 42 h hypoxia caused alternative polarization of murine PMs with significant arginase prevalence. NSC631570 repolarized arginine metabolism of hypoxic macrophages to NOS dominant and activated their pro-inflammatory functions: recovered ROS production and increased alarmin releaseNSC631570 can restore pro-inflammatory functions of macrophages, alternatively polarized by hypoxia.ΠΠΈΠΏΠΎΠΊΡΠΈΡ ΡΠ²Π»ΡΠ΅ΡΡΡ Π²Π°ΠΆΠ½ΡΠΌ ΡΠ°ΠΊΡΠΎΡΠΎΠΌ ΠΌΠΈΠΊΡΠΎΠΎΠΊΡΡΠΆΠ΅Π½ΠΈΡ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ². ΠΠ½ΠΎΠ³ΠΈΠ΅ ΡΠΈΠ·ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈ ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΏΡΠΎΡΠ΅ΡΡΡ, Π² ΡΠΎΠΌ ΡΠΈΡΠ»Π΅ ΡΠΎΡΡ ΡΠΎΠ»ΠΈΠ΄Π½ΡΡ
ΠΎΠΏΡΡ
ΠΎΠ»Π΅ΠΉ, Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΠ·ΡΡΡΡΡ Π½ΠΈΠ·ΠΊΠΈΠΌ Π΄Π°Π²Π»Π΅Π½ΠΈΠ΅ΠΌ ΠΊΠΈΡΠ»ΠΎΡΠΎΠ΄Π° ΠΈ ΠΏΡΠΈΡΡΡΡΡΠ²ΠΈΠ΅ΠΌ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ². ΠΠΏΡΡ
ΠΎΠ»Π΅Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½Π°Ρ Π³ΠΈΠΏΠΎΠΊΡΠΈΡ ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΎΠ΄Π½ΠΎΠΉ ΠΈΠ· ΠΏΡΠΈΡΠΈΠ½ Π°Π»ΡΡΠ΅ΡΠ½Π°ΡΠΈΠ²Π½ΠΎΠΉ ΠΏΠΎΠ»ΡΡΠΈΠ·Π°ΡΠΈΠΈ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ² Π² ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ, ΠΏΡΠ΅Π²ΡΠ°ΡΠ°Ρ ΠΈΡ
Π² ΠΊΠ»Π΅ΡΠΊΠΈ-ΡΠΎΡΠ·Π½ΠΈΠΊΠΈ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠ³ΠΎ ΠΏΡΠΎΡΠ΅ΡΡΠ°. Π¦Π΅Π»ΡΡ ΡΠ°Π±ΠΎΡΡ Π±ΡΠ»ΠΎ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ Π²Π»ΠΈΡΠ½ΠΈΡ NSC631570 β ΠΎΠΏΡΡ
ΠΎΠ»Π΅-ΡΠ΅Π»Π΅ΠΊΡΠΈΠ²Π½ΠΎΠ³ΠΎ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ° ΡΠΎ ΡΠΏΠΎΡΠΎΠ±Π½ΠΎΡΡΡΡ ΠΈΠ·Π±ΠΈΡΠ°ΡΠ΅Π»ΡΠ½ΠΎ Π½Π°ΠΊΠ°ΠΏΠ»ΠΈΠ²Π°ΡΡΡΡ Π² ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ β Π½Π° ΡΡΠ½ΠΊΡΠΈΠΈ Π³ΠΈΠΏΠΎΠΊΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ². ΠΡΡΠΈΠ½ΡΠ΅ ΠΏΠ΅ΡΠΈΡΠΎΠ½Π΅Π°Π»ΡΠ½ΡΠ΅ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΈ (ΠΠ) ΠΏΠΎΠ΄Π²Π΅ΡΠ³Π°Π»ΠΈΡΡ Π³ΠΈΠΏΠΎΠΊΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΎΠ±ΡΠ°Π±ΠΎΡΠΊΠ΅ (3 % Oβ). Π£ΡΠΎΠ²Π΅Π½Ρ Π½ΠΈΡΡΠΈΡΠΎΠ² ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π»ΠΈ Π² ΡΠ΅Π°ΠΊΡΠΈΠΈ ΠΡΠΈΡΡΠ°. ΠΡΠ³ΠΈΠ½Π°Π·Π½ΡΡ Π°ΠΊΡΠΈΠ²-Π½ΠΎΡΡΡ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ ΠΊΠΎΠ»ΠΎΡΠΈΠΌΠ΅ΡΡΠΈΡΠ΅ΡΠΊΠΈΠΌ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ. ΠΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΠ΅ Π²Π½ΡΡΡΠΈΠΊΠ»Π΅ΡΠΎΡΠ½ΡΡ
ΡΠ΅Π°ΠΊΡΠΈΠ²Π½ΡΡ
ΡΠΎΡΠΌ ΠΊΠΈΡΠ»ΠΎΡΠΎΠ΄Π° (Π Π€Π) ΠΈ ΡΠ°Π³ΠΎΡΠΈΡΠΎΠ· Π°Π½Π°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°Π»ΠΈ c ΠΏΠΎΠΌΠΎΡΡΡ ΠΏΡΠΎΡΠΎΡΠ½ΠΎΠΉ ΡΠΈΡΠΎΡΠ»ΡΠΎΡΠΈΠΌΠ΅ΡΡΠΈΠΈ. ΠΠ½Π΅ΠΊΠ»Π΅ΡΠΎΡΠ½ΡΡ ΠΏΡΠΎΠ΄ΡΠΊΡΠΈΡ Π Π€Π ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ Π² ΠΠ‘Π’-ΡΠ΅ΡΡΠ΅, ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡ HMGB1 β ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ELISA. 42-ΡΠ°ΡΠΎΠ²Π°Ρ Π³ΠΈΠΏΠΎΠΊΡΠΈΡ ΠΎΠ±ΡΡΠ»ΠΎΠ²Π»ΠΈΠ²Π°Π»Π° Π°Π»ΡΡΠ΅ΡΠ½Π°ΡΠΈΠ²Π½ΡΡ ΠΏΠΎΠ»ΡΡΠΈΠ·Π°ΡΠΈΡ ΠΠ Ρ ΠΏΡΠ΅ΠΎΠ±Π»Π°Π΄Π°Π½ΠΈΠ΅ΠΌ Π°ΡΠ³ΠΈΠ½Π°Π·Π½ΠΎΠΉ Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΠΈ. NSC631570 Π²ΡΠ·ΡΠ²Π°Π» ΡΠ΅ΠΏΠΎΠ»ΡΡΠΈΠ·Π°ΡΠΈΡ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° Π°ΡΠ³ΠΈΠ½ΠΈΠ½Π° Π² Π³ΠΈΠΏΠΎΠΊΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΠ ΠΈ Π°ΠΊΡΠΈΠ²ΠΈΡΠΎΠ²Π°Π» ΠΈΡ
ΠΏΡΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΡΠ΅ ΡΡΠ½ΠΊΡΠΈΠΈ: ΡΡΠΈΠ»ΠΈΠ²Π°Π» ΠΊΠΈΡΠ»ΠΎΡΠΎΠ΄-Π·Π°Π²ΠΈΡΠΈΠΌΡΠΉ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌ ΠΈ Π²ΡΠ΄Π΅Π»Π΅Π½ΠΈΠ΅ Π°Π»Π°ΡΠΌΠΈΠ½ΠΎΠ². NSC631570 ΡΠΏΠΎΡΠΎΠ±Π΅Π½ Π²ΠΎΡΡΡΠ°Π½Π°Π²Π»ΠΈΠ²Π°ΡΡ ΠΏΡΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΡΠ΅ ΡΡΠ½ΠΊΡΠΈΠΈ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ², Π°Π»ΡΡΠ΅ΡΠ½Π°ΡΠΈΠ²Π½ΠΎ ΠΏΠΎΠ»ΡΡΠΈΠ·ΠΎΠ²Π°Π½Π½ΡΡ
Π³ΠΈΠΏΠΎΠΊΡΠΈΠ΅ΠΉ.ΠΡΠΏΠΎΠΊΡΡΡ Ρ Π²Π°ΠΆΠ»ΠΈΠ²ΠΈΠΌ ΡΠ°ΠΊΡΠΎΡΠΎΠΌ ΠΌΡΠΊΡΠΎΠΎΡΠΎΡΠ΅Π½Π½Ρ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΡΠ². ΠΠ°Π³Π°ΡΠΎ Π²Π°ΠΆΠ»ΠΈΠ²ΠΈΡ
ΡΡΠ·ΡΠΎΠ»ΠΎΠ³ΡΡΠ½ΠΈΡ
Ρ ΠΏΠ°ΡΠΎ-Π»ΠΎΠ³ΡΡΠ½ΠΈΡ
ΠΏΡΠΎΡΠ΅ΡΡΠ², Ρ ΡΠΎΠΌΡ ΡΠΈΡΠ»Ρ ΡΡΡΡ ΡΠΎΠ»ΡΠ΄Π½ΠΈΡ
ΠΏΡΡ
Π»ΠΈΠ½, Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΠ·ΡΡΡΡΡΡ Π½ΠΈΠ·ΡΠΊΠΈΠΌ ΡΠΈΡΠΊΠΎΠΌ ΠΊΠΈΡΠ½Ρ Ρ ΠΏΡΠΈΡΡΡΠ½ΡΡΡΡ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΡΠ². ΠΡΡ
Π»ΠΈΠ½ΠΎ-Π°ΡΠΎΡΡΠΉΠΎΠ²Π°Π½Π° Π³ΡΠΏΠΎΠΊΡΡΡ Ρ ΠΎΠ΄Π½ΡΡΡ Π· ΠΏΡΠΈΡΠΈΠ½ Π°Π»ΡΡΠ΅ΡΠ½Π°ΡΠΈΠ²Π½ΠΎΡ ΠΏΠΎΠ»ΡΡΠΈΠ·Π°ΡΡΡ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΡΠ² Ρ ΠΏΡΡ
Π»ΠΈΠ½Π½ΡΠΉ ΡΠΊΠ°Π½ΠΈΠ½Ρ, ΠΏΠ΅ΡΠ΅ΡΠ²ΠΎΡΡ-ΡΡΠΈ ΡΡ
Π½Π° ΠΊΠ»ΡΡΠΈΠ½ΠΈ-ΡΠΎΡΠ·Π½ΠΈΠΊΠΈ ΠΏΡΡ
Π»ΠΈΠ½Π½ΠΎΠ³ΠΎ ΠΏΡΠΎΡΠ΅ΡΡ. ΠΠ΅ΡΠΎΡ ΡΠΎΠ±ΠΎΡΠΈ Π±ΡΠ»ΠΎ Π΄ΠΎΡΠ»ΡΠ΄ΠΆΠ΅Π½Π½Ρ Π²ΠΏΠ»ΠΈΠ²Ρ NSC631570 β ΠΏΡΡ
Π»ΠΈΠ½ΠΎ-ΡΠ΅Π»Π΅ΠΊΡΠΈΠ²Π½ΠΎΠ³ΠΎ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ Π·Ρ Π·Π΄Π°ΡΠ½ΡΡΡΡ Π²ΠΈΠ±ΡΡΠΊΠΎΠ²ΠΎ Π½Π°ΠΊΠΎΠΏΠΈΡΡΠ²Π°ΡΠΈΡΡ Ρ ΠΏΡΡ
Π»ΠΈΠ½Π½ΡΠΉ ΡΠΊΠ°Π½ΠΈΠ½Ρ β Π½Π° ΡΡΠ½ΠΊΡΡΡ Π³ΡΠΏΠΎΠΊΡΠΈΡΠ½ΠΈΡ
ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΡΠ². ΠΠΈΡΠ°ΡΡ ΠΏΠ΅ΡΠΈΡΠΎΠ½Π΅Π°Π»ΡΠ½Ρ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΈ (ΠΠ) ΠΏΡΠ΄Π΄Π°Π²Π°Π»ΠΈΡΡ Π³ΡΠΏΠΎΠΊΡΠΈΡΠ½ΡΠΉ ΠΎΠ±ΡΠΎΠ±ΡΡ (3 % Oβ). Π ΡΠ²Π΅Π½Ρ Π½ΡΡΡΠΈΡΡΠ² Π²ΠΈΠ²ΡΠ°Π»ΠΈ Π² ΡΠ΅Π°ΠΊΡΡΡ ΠΡΡΡΠ°. ΠΡΠ³ΡΠ½Π°Π·Π½Ρ Π°ΠΊΡΠΈΠ²Π½ΡΡΡΡ Π²ΠΈΠ·Π½Π°ΡΠ°Π»ΠΈ ΠΊΠΎΠ»ΠΎΡΠΈΠΌΠ΅ΡΡΠΈΡΠ½ΠΈΠΌ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ. Π£ΡΠ²ΠΎΡΠ΅Π½Π½Ρ Π²Π½ΡΡΡΡΡΠ½ΡΠΎΠΊΠ»ΡΡΠΈΠ½Π½ΠΈΡ
ΡΠ΅Π°ΠΊΡΠΈΠ²Π½ΠΈΡ
ΡΠΎΡΠΌ ΠΊΠΈΡΠ½Ρ (Π Π€Π) Ρ ΡΠ°Π³ΠΎΡΠΈΡΠΎΠ· Π°Π½Π°Π»ΡΠ·ΡΠ²Π°Π»ΠΈ Π·Π° Π΄ΠΎΠΏΠΎΠΌΠΎΠ³ΠΎΡ ΠΏΡΠΎΡΠΎΡΠ½ΠΎΡ ΡΠΈΡΠΎΡΠ»ΡΠΎΡΠΈΠΌΠ΅ΡΡΡΡ. ΠΠΎΠ·Π°ΠΊΠ»ΡΡΠΈΠ½Π½Ρ ΠΏΡΠΎΠ΄ΡΠΊΡΡΡ Π Π€Π Π²ΠΈΠ·Π½Π°ΡΠ°Π»ΠΈ Π² ΠΠ‘Π’-ΡΠ΅ΡΡΡ, Π΅ΠΊΡΠΏΡΠ΅ΡΡΡ HMGB1 β ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ELISA. 42-Π³ΠΎΠ΄ΠΈΠ½Π½Π° Π³ΡΠΏΠΎΠΊΡΡΡ ΡΠΏΡΠΈΡΠΈΠ½ΡΠ»Π° Π°Π»ΡΡΠ΅ΡΠ½Π°ΡΠΈΠ²Π½Ρ ΠΏΠΎΠ»ΡΡΠΈ-Π·Π°ΡΡΡ ΠΠ Π· ΠΏΠ΅ΡΠ΅Π²Π°ΠΆΠ°Π½Π½ΡΠΌ Π°ΡΠ³ΡΠ½Π°Π·Π½ΠΎΡ Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ. NSC631570 Π²ΠΈΠΊΠ»ΠΈΠΊΠ°Π² ΡΠ΅ΠΏΠΎΠ»ΡΡΠΈΠ·Π°ΡΡΡ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΡΠ·ΠΌΡ Π°ΡΠ³ΡΠ½ΡΠ½Ρ Ρ Π³ΡΠΏΠΎΠΊΡΠΈΡΠ½ΠΈΡ
ΠΠ Ρ Π°ΠΊΡΠΈΠ²ΡΠ²Π°Π² ΡΡ
ΠΏΡΠΎΠ·Π°ΠΏΠ°Π»ΡΠ½Ρ ΡΡΠ½ΠΊΡΡΡ: ΠΏΠΎΡΠΈΠ»ΡΠ²Π°Π² ΠΊΠΈΡΠ½Π΅Π·Π°Π»Π΅ΠΆΠ½ΠΈΠΉ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΡΠ·ΠΌ Ρ Π²ΠΈΠ΄ΡΠ»Π΅Π½Π½Ρ Π°Π»Π°ΡΠΌΡΠ½ΡΠ². NSC631570 Π·Π΄Π°ΡΠ½ΠΈΠΉ Π²ΡΠ΄Π½ΠΎΠ²Π»ΡΠ²Π°ΡΠΈ ΠΏΡΠΎΠ·Π°ΠΏΠ°Π»ΡΠ½Ρ ΡΡΠ½ΠΊΡΡΡ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΡΠ², Π°Π»ΡΡΠ΅ΡΠ½Π°ΡΠΈΠ²Π½ΠΎ ΠΏΠΎΠ»ΡΡΠΈΠ·ΠΎΠ²Π°Π½ΠΈΡ
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