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Yu W.,Tianjin First Center Hospital | Sheng M.,Tianjin First Center Hospital | Xu R.,Tianjin First Center Hospital | Yu J.,Tianjin Chest Hospital | And 6 more authors.
Journal of Translational Medicine | Year: 2013

Background: Ischemia/reperfusion injury plays a crucial role in renal transplantation, and represents a significant risk factor for acute renal failure and delayed graft function. The pathophysiological contribution of endoplasmic reticulum and mitochondria stress to ischemia/reperfusion injury has also been highlighted. Berberine (BBR) has been showed to attenuate ischemia/reperfusion injury by inhibiting oxidative stress. The study was carried out to investigate whether the pretreatment of BBR could reduce hypoxia/reoxygenation (H/R)-induced injury by inhibiting mitochondria stress and endoplasmic reticulum stress pathways. Methods: The cultured human renal proximal tubular cell line HK-2 cells were exposed to 24 h hypoxia (5% CO2, 1% O2, 94% N2) followed by 3 h reoxygenation (5% CO2, 21% O2, 74% N2). And BBR was added to the culture medium 2h prior to the treatment. Then the cell viability, oxidative stress level, morphological change of apoptosis and apoptotic rate were determined. In addition, Western blot analysis was performed to identify the expression of apoptotic pathway parameters, including Bcl-2, Bax and cytochrome C involved in mitochondrial-dependent pathway and ER stress hallmarks such as glucose-regulated protein 78 and CCAAT/enhancer binding protein homologous protein. Results: H/R produced dramatic injuries in HK-2 cells. The cell viability and the oxidative stress level in group H/R was significantly decreased. The classical morphological change of apoptosis was found, while the apoptotic rate and the expression of proteins involved in mitochondrial stress and endoplasmic reticulum stress pathways increased (p<0.05). Administration of BBR significantly inhibited these H/R induced changes (p<0.05). Conclusion: This study revealed that BBR pretreatment serves a protective role against H/R induced apoptosis of human renal proximal tubular cells, and the mechanism is related to suppression of mitochondrial stress and endoplasmic reticulum stress pathways. © 2013 Yu et al; licensee BioMed Central Ltd.


Chen L.,First Central Hospital of Tianjin | Feng X.,First Central Hospital of Tianjin | Wang Y.,Key Laboratory for Critical Care Medicine of the Ministry of Health | Xu X.,Key Laboratory for Critical Care Medicine of the Ministry of Health | And 3 more authors.
Transplantation Proceedings | Year: 2016

Background From the medical and ethical points of view, donation after brain death is a more acceptable organ source than that from a living donor because it has the advantage of providing multiple organs from a single donor source. Hence, it has become a more promising field of research which focuses on the protection of organs at brain death Here we investigated the role of transforming growth factor (TGF)-β1 in a porcine model of brain death. Methods A porcine model of brain death was established by increasing the intracranial pressure (ICP) after which TGF-β1 was monitored by immunofluorescence at the following time points: before ICP was performed (t1), at brain death (t2), and at 3 (t3), 6 (t4), 9 (t5), and 18 (t6) hours after brain death. The data were analyzed using the fixed effect regression method and the correlation between the results was determined by Pearson analysis. Results Our results showed that there was a significant increase in the levels of TGF-β1 (P <.05), urea (P <.01), creatinine (P <.01), and aspartate aminotransferase (AST; P <.01) during the 18-hour brain death process. There were negative correlations between TGF-β1 and urea, creatinine, alanine aminotransferase, AST, and total bilirubin. The negative correlations between TGF-β1 and creatinine and AST achieved statistical significance (P <.05). Conclusions These findings taken together confirm that significant damages are caused to the myocardial fiber cell and kidney glomerulus during brain death process, and that TGF-β1 is associated with the protection of these organs. © 2016 Elsevier Inc.


PubMed | Key Laboratory for Critical Care Medicine of the Ministry of Health, Tianjin Medical University and Tianjin First Central Hospital
Type: Journal Article | Journal: Annals of clinical and laboratory science | Year: 2016

To investigate the effects of microRNA-506 (miR-506) on malignancy of colorectal carcinoma (CRC) cells and to elucidate the underlying mechanism.Human colorectal carcinoma cell lines SW480, SW620, HCT116, and HT29 were served as model. Five experimental groups are established in this study, including cell control, pcDNA3 blank vector control, miR-506 over-expression, pSIH1 blank vector control, and miR-506 suppression groups. Quantitative reverse transcription PCR (qRT-PCR) assay was performed to measure miR-506 level. Transwell, Cell counting kit8 (CCK-8), and colony formation assays were performed to detect migration and invasion, viability, and colony formation abilities of CRC cell lines, respectively. Furthermore, bioinformatics method was applied to predict potential target genes of miR-506. Green fluorescent protein (GFP) reporter assays were used to verify the direct regulation of miR-506 on target mRNA in CRC cell lines. The LAMC1 mRNA and protein levels were detected by qRT-PCR and Western blot, respectively.In the CRC cell lines, miR-506 level increased in the miR-506 over-expression group (P<0.05), compared with the blank vector control group. In the miR-506 over-expression group, cellular viability was significantly reduced (P<0.05). Migrated and invasive cell numbers and cell colony numbers were decreased (P<0.05). LAMC1 mRNA and protein levels in the miR-506 over-expression groups were lower than those in the control groups (P<0.05). However, there were no difference on the above indexes between pSIH1 blank vector control and miR-506 suppression groups.miR-506 acts as a tumor suppressor and inhibits malignancy of colorectal cancer cells through directly targeting LAMC1.


PubMed | Key Laboratory for Critical Care Medicine of the Ministry of Health and The First Central Hospital of Tianjin
Type: Journal Article | Journal: Transplantation proceedings | Year: 2016

From the medical and ethical points of view, donation after brain death is a more acceptable organ source than that from a living donor because it has the advantage of providing multiple organs from a single donor source. Hence, it has become a more promising field of research which focuses on the protection of organs at brain death Here we investigated the role of transforming growth factor (TGF)-1 in a porcine model of brain death.A porcine model of brain death was established by increasing the intracranial pressure (ICP) after which TGF-1 was monitored by immunofluorescence at the following time points: before ICP was performed (t1), at brain death (t2), and at 3 (t3), 6 (t4), 9 (t5), and 18 (t6) hours after brain death. The data were analyzed using the fixed effect regression method and the correlation between the results was determined by Pearson analysis.Our results showed that there was a significant increase in the levels of TGF-1 (P < .05), urea (P < .01), creatinine (P < .01), and aspartate aminotransferase (AST; P < .01) during the 18-hour brain death process. There were negative correlations between TGF-1 and urea, creatinine, alanine aminotransferase, AST, and total bilirubin. The negative correlations between TGF-1 and creatinine and AST achieved statistical significance (P < .05).These findings taken together confirm that significant damages are caused to the myocardial fiber cell and kidney glomerulus during brain death process, and that TGF-1 is associated with the protection of these organs.

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