We studied on hematological parameters, lymphocytes distribution and stem cell (CD34 positive) count from cord blood of 43 healthy newborn at obstetrics department, Bach Mai hospital. The result showed that, stem cell count of cord blood is high (16.2% of nucleated cell, equal to 2.4+/- 0.3 G/l). this will be useful to allegoric stem cell transplantation. However, relatively high count of white cell (especially T lymphocyte) can be considerable to procedure and transplant result, free of graft versus host disease.
Fetal Blood ; Bone Marrow Transplantation

Background: The reduction of erythrocytes from cord blood is very need for long - term storage of C034 cells for transplantation. Reduced erythrocyte will reduces preservative blood volume, preservatives and freely HST when defrosting, so stem cells are better protected. Objectives: To study selection of the best centrifugal procedure to reduce maximal erythrocytes and lose minimal C034 cells from cord blood. Subjects and methods: 20 blood samples selected from 60 cord blood units was used for this study. The study was carried out through two steps. In the first step, the centrifugal speed was fixed and the centrifugal time was changed.In the second step, the centrifugal time was fixed, the centrifugal speed was changed. From collected results the best appropriate procedure to reduce erythrocytes from cord blood have been selected. Results: The procedure of gradient centrifuge with speed of 500g in 6 minutes isolated> 50% of erythrocytes, kept > 84% of CD34 cells and then centrifuge of 1000 g in 10 minutes reduced about 40% of volume of nuclear cell - suspension. Conclusion: The procedure can use for preparation of stem cell suspension from cord blood to storage in nitrogen liquid. \r\n', u'\r\n', u'
Erythrocytes/ pathology ; Fetal Blood/ chemistry ; drug effects ; immunology

Balanophora laxiflora Hemsl. (Balanophoraceae) is a traditional medicinal plant with a diverse array of biological activities. In our exploration of new bioactive constituents from B. laxiflora, we isolated five compounds, including a new lignan, balanophorone (5), and four known phenolic compounds (1–4). The chemical structures of these compounds were determined by extensive spectroscopic analyses, including 1D and 2D NMR, HR-ESI-MS, and CD. In addition, we evaluated the effects of each of the isolates (1–5) on the messenger RNA expression levels of tumor necrosis factor (TNF)-α and cyclooxygenase (COX)-2 in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and cytotoxicity against MCF-7 and MDA-MB-231 breast cancer cells. Compound 2 showed significant inhibition of LPS-induced COX-2 and TNF-α expression in RAW 264.7 macrophages, while compound 4 showed moderate cytotoxicity against MCF-7 and MDA-MB-231 breast cancer cells, with IC 50 values of 18.3 and 30.7 μM, respectively. No significant effects on the viability of normal mammary epithelial cells were observed.

Balanophora laxiflora Hemsl. (Balanophoraceae) is a traditional medicinal plant with a diverse array of biological activities. In our exploration of new bioactive constituents from B. laxiflora, we isolated five compounds, including a new lignan, balanophorone (5), and four known phenolic compounds (1–4). The chemical structures of these compounds were determined by extensive spectroscopic analyses, including 1D and 2D NMR, HR-ESI-MS, and CD. In addition, we evaluated the effects of each of the isolates (1–5) on the messenger RNA expression levels of tumor necrosis factor (TNF)-α and cyclooxygenase (COX)-2 in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and cytotoxicity against MCF-7 and MDA-MB-231 breast cancer cells. Compound 2 showed significant inhibition of LPS-induced COX-2 and TNF-α expression in RAW 264.7 macrophages, while compound 4 showed moderate cytotoxicity against MCF-7 and MDA-MB-231 breast cancer cells, with IC 50 values of 18.3 and 30.7 μM, respectively. No significant effects on the viability of normal mammary epithelial cells were observed.

Background: Dipeptidyl peptidase-4 inhibitors (DPP-4Is) are used clinically as oral antidiabetic agents. Although DPP-4Is are known to ameliorate liver fibrosis, the protective mechanism of DPP-4Is in liver fibrosis remains obscure. In this study, gemigliptin was used to investigate the potential of DPP-4Is to alleviate the progression of liver fibrosis. Methods: To clarify the effects and mechanisms of gemigliptin, we conducted various experiments in LX-2 cells (immortalized human hepatic stellate cells [HSCs], the principal effectors of hepatic fibrogenesis), which were activated by succinate and exhibited elevated expression of α-smooth muscle actin, collagen type 1, and pro-inflammatory cytokines and increased cell proliferation. In vivo, we examined the effects and mechanisms of gemigliptin on a high-fat, high-cholesterol–induced mouse model of nonalcoholic steatohepatitis (NASH). Results: Gemigliptin decreased the expression of fibrogenesis markers and reduced the abnormal proliferation of HSCs. In addition, gemigliptin reduced the succinate-induced production of mitochondrial reactive oxygen species (ROS), intracellular ROS, and mitochondrial fission in HSCs. Furthermore, in the mouse model of NASH-induced liver fibrosis, gemigliptin alleviated both liver fibrosis and mitochondrial dysfunction. Conclusion Gemigliptin protected against HSC activation and liver fibrosis by alleviating mitochondrial dysfunction and ROS production, indicating its potential as a strategy for preventing the development of liver disease.

Background: Hepatic stellate cells (HSCs) are the central players interacting with multiple cell types in liver fibrosis. The crosstalk between HSCs and macrophages has recently become clearer. Irisin, an exercise-responsive myokine, was known to have a potentially protective role in liver and renal fibrosis, especially in connection with stellate cells. This study investigated the effects of irisin on the interaction between HSCs and macrophages. Methods: Tamm-Horsfall protein-1 (THP-1) human monocytes were differentiated into macrophages, polarized into the inflammatory M1 phenotype with lipopolysaccharide. Lieming Xu-2 (LX-2) cells, human HSCs, were treated with conditioned media (CM) from M1 macrophages, with or without recombinant irisin. HSCs responses to CM from M1 macrophages were evaluated regarding activation, proliferation, wound healing, trans-well migration, contractility, and related signaling pathway. Results: CM from M1 macrophages significantly promoted HSC proliferation, wound healing, transwell migration, and contractility, but not activation of HSCs. Irisin co-treatment attenuated these responses of HSCs to CM. However, CM and irisin treatment did not induce any changes in HSC activation. Further, irisin co-treatment alleviated CM-induced increase of phopho-protein kinase B (pAKT), matrix metalloproteinase-9 (MMP-9), and tissue inhibitor of metalloproteinases-1 (TIMP-1). Conclusion These findings suggested that irisin may play a protective role in the pathogenesis of liver fibrosis, especially when working in the crosstalk between HSCs and macrophages.

Dry eye disease (DED) is a complicated disorder that impacts ocular surface and tear-film stability. Inflammation has recently been reported as the core mechanism and main therapeutic target of DED. Although anti-inflammatory drugs have been developed, they still have limited efficacy and various side effects. Recent reports have suggested that kinase inhibitors are beneficial for relieving inflammation. Therefore, this study aimed to investigate the anti-inflammatory effects of LCB 03-0110, a multi-tyrosine kinase inhibitor, on representative cell-based models (HCE-2 and Th17 cells) of DED. While tacrolimus and tofacitinib, two different anti-inflammatory drugs that have entered clinical trials for DED treatment, did not induce any anti-inflammatory responses in HCE-2 cells, LCB 03-0110 significantly suppressed the phosphorylation of P38 and ERK and reduced the expression levels of IL-6 and IL-8 in HCE-2 cells treated with either LPS or poly(I:C). Moreover, LCB 03-0110 notably decreased the expression level of IL-17A in Th17 cells in a dose-dependent manner, whereas tofacitinib promoted IL-17A production at low concentrations but inhibited its expression at concentrations greater than 1 μM. In addition, LCB 03-0110 was found to be non-toxic to both HCE-2 and Th17 cells. In conclusion, these results suggest that LCB 03-0110 would be a promising drug candidate for the treatment of DED because of its advantages over tacrolimus and tofacitinib.

Dry eye disease (DED) is a complicated disorder that impacts ocular surface and tear-film stability. Inflammation has recently been reported as the core mechanism and main therapeutic target of DED. Although anti-inflammatory drugs have been developed, they still have limited efficacy and various side effects. Recent reports have suggested that kinase inhibitors are beneficial for relieving inflammation. Therefore, this study aimed to investigate the anti-inflammatory effects of LCB 03-0110, a multi-tyrosine kinase inhibitor, on representative cell-based models (HCE-2 and Th17 cells) of DED. While tacrolimus and tofacitinib, two different anti-inflammatory drugs that have entered clinical trials for DED treatment, did not induce any anti-inflammatory responses in HCE-2 cells, LCB 03-0110 significantly suppressed the phosphorylation of P38 and ERK and reduced the expression levels of IL-6 and IL-8 in HCE-2 cells treated with either LPS or poly(I:C). Moreover, LCB 03-0110 notably decreased the expression level of IL-17A in Th17 cells in a dose-dependent manner, whereas tofacitinib promoted IL-17A production at low concentrations but inhibited its expression at concentrations greater than 1 μM. In addition, LCB 03-0110 was found to be non-toxic to both HCE-2 and Th17 cells. In conclusion, these results suggest that LCB 03-0110 would be a promising drug candidate for the treatment of DED because of its advantages over tacrolimus and tofacitinib.

Dry eye disease (DED) is a complicated disorder that impacts ocular surface and tear-film stability. Inflammation has recently been reported as the core mechanism and main therapeutic target of DED. Although anti-inflammatory drugs have been developed, they still have limited efficacy and various side effects. Recent reports have suggested that kinase inhibitors are beneficial for relieving inflammation. Therefore, this study aimed to investigate the anti-inflammatory effects of LCB 03-0110, a multi-tyrosine kinase inhibitor, on representative cell-based models (HCE-2 and Th17 cells) of DED. While tacrolimus and tofacitinib, two different anti-inflammatory drugs that have entered clinical trials for DED treatment, did not induce any anti-inflammatory responses in HCE-2 cells, LCB 03-0110 significantly suppressed the phosphorylation of P38 and ERK and reduced the expression levels of IL-6 and IL-8 in HCE-2 cells treated with either LPS or poly(I:C). Moreover, LCB 03-0110 notably decreased the expression level of IL-17A in Th17 cells in a dose-dependent manner, whereas tofacitinib promoted IL-17A production at low concentrations but inhibited its expression at concentrations greater than 1 μM. In addition, LCB 03-0110 was found to be non-toxic to both HCE-2 and Th17 cells. In conclusion, these results suggest that LCB 03-0110 would be a promising drug candidate for the treatment of DED because of its advantages over tacrolimus and tofacitinib.

Dry eye disease (DED) is a complicated disorder that impacts ocular surface and tear-film stability. Inflammation has recently been reported as the core mechanism and main therapeutic target of DED. Although anti-inflammatory drugs have been developed, they still have limited efficacy and various side effects. Recent reports have suggested that kinase inhibitors are beneficial for relieving inflammation. Therefore, this study aimed to investigate the anti-inflammatory effects of LCB 03-0110, a multi-tyrosine kinase inhibitor, on representative cell-based models (HCE-2 and Th17 cells) of DED. While tacrolimus and tofacitinib, two different anti-inflammatory drugs that have entered clinical trials for DED treatment, did not induce any anti-inflammatory responses in HCE-2 cells, LCB 03-0110 significantly suppressed the phosphorylation of P38 and ERK and reduced the expression levels of IL-6 and IL-8 in HCE-2 cells treated with either LPS or poly(I:C). Moreover, LCB 03-0110 notably decreased the expression level of IL-17A in Th17 cells in a dose-dependent manner, whereas tofacitinib promoted IL-17A production at low concentrations but inhibited its expression at concentrations greater than 1 μM. In addition, LCB 03-0110 was found to be non-toxic to both HCE-2 and Th17 cells. In conclusion, these results suggest that LCB 03-0110 would be a promising drug candidate for the treatment of DED because of its advantages over tacrolimus and tofacitinib.