Curcumin suppresses PPARδ expression and related genes in HT-29 cells

AIM:To investigate the effects of curcumin on the expression of peroxisome proliferator-activated receptorδ(PPARδ)and related genes in HT-29 cells. METHODS:HT-29 cells were treated with curcumin (0-80μmol/L)for 24 h.The effects of curcumin on the morphology of HT-29 cells were studied by Hoechst 33342 staining.The activity of caspase-3 was determined using DEVD-p NA as substrate.The levels of peroxisome PPARδ,14-3-3εand vascular endothelial growth factor(VEGF)in HT-29 cells were determined by Western blotting analysis and their mRNA expression was determined by real-time quantitative RT-PCR. RESULTS:Treatment with 10-80μmol/L curcumin induced typical features of apoptosis and activated the caspase-3 in HT-29 cells.The expression of PPARδ, 14-3-3εand VEGF was reduced and the activity of β-catenin/Tcf-4 signaling was inhibited by curcumin treatment. CONCLUSION:Curcumin can induce apoptosis of HT-29 cells and down-regulate the expression of PPARδ,14-3-3εand VEGF in HT-29.

Firebird stent for the treatment of patients with coronary heart disease： short-term clinical outcome

sirolimus-eluting stent (SES ) 戏剧性地减少了的目的有 .This 学习试图与冠的心疾病(CHD ) 为病人评估鲜艳的小鸟 stent 培植的短期的功效和安全的赤裸金属的 stent (BMS ) 的与那相比的率 ofrestenosis。从通过 2007 年 7 月的 Apri12006 的方法， 155 个病人(意味着年龄 58.9310.27 年) 在 Daxing 与鲜艳的小鸟 stent 或密码精选 stent 与 CHD 被植入医院。病人们被跟随在上面为一年。所有原因死亡，主要不利心脏的事件(向，包括的心脏的死亡，心肌的梗塞，心绞痛的复发，心失败， revascularization，和不利心律不齐) 和 stent 血栓在 2 个组之间被比较。155 个连续病人，的结果 147 个病人完全是 revascularized。这些病人， 48 (与 59 损害) 与鲜艳的小鸟 stent 被对待， 59 个病人(与 75 损害) 与密码精选 stent。人口统计的特征在 2 个组是类似的。所有 angiographic 和程序的结果不在 2 个组之间是显著地不同的。所有原因死亡，心肌的梗塞，心绞痛的复发，向和 stent 血栓以前在 2 个组之间是几乎相同的分泌物，在 6 个月并且在一年 .Conclusion ，鲜艳的小鸟 stent 的短期的功效和安全类似于密码的为有 CHD 的病人的治疗的精选 stent 。

Effect of ginsenoside Rg1 on hematopoietic stem cells in treating aplastic anemia in mice via MAPK pathway

BACKGROUND Aplastic anemia(AA)presents a significant clinical challenge as a life-threatening condition due to failure to produce essential blood cells,with the current the-rapeutic options being notably limited.AIM To assess the therapeutic potential of ginsenoside Rg1 on AA,specifically its protective effects,while elucidating the mechanism at play.METHODS We employed a model of myelosuppression induced by cyclophosphamide(CTX)in C57 mice,followed by administration of ginsenoside Rg1 over 13 d.The invest-igation included examining the bone marrow,thymus and spleen for pathological changes via hematoxylin-eosin staining.Moreover,orbital blood of mice was collected for blood routine examinations.Flow cytometry was employed to identify the impact of ginsenoside Rg1 on cell apoptosis and cycle in the bone marrow of AA mice.Additionally,the study further evaluated cytokine levels with enzyme-linked immunosorbent assay and analyzed the expression of key proteins in the MAPK signaling pathway via western blot.RESULTS Administration of CTX led to significant damage to the bone marrow’s structural integrity and a reduction in hematopoietic cells,establishing a model of AA.Ginsenoside Rg1 successfully reversed hematopoietic dysfunction in AA mice.In comparison to the AA group,ginsenoside Rg1 provided relief by reducing the induction of cell apoptosis and inflammation factors caused by CTX.Furthermore,it helped alleviate the blockade in the cell cycle.Treatment with ginsenoside Rg1 significantly alleviated myelosuppression in mice by inhibiting the MAPK signaling pathway.CONCLUSION This study suggested that ginsenoside Rg1 addresses AA by alleviating myelosuppression,primarily through modulating the MAPK signaling pathway,which paves the way for a novel therapeutic strategy in treating AA,highlighting the potential of ginsenoside Rg1 as a beneficial intervention.

Curcumin induces apoptosis through the mitochondria-mediated apoptotic pathway in HT-29 cells

Objective: To investigate the effects of curcumin on release of cytochrome c and expressions of Bcl-2, Bax, Bad, Bcl-xL, caspase-3, poly ADP-ribose polymerase (PARP), and survivin of HT-29 cells. Methods: HT-29 cells were treated with curcumin (0～80 μmol/L) for 24 h. The release of cytochrome c from the mitochondria and the apoptosis-related proteins Bax, Bcl-2, Bcl-xL, Bad, caspase-3, PARP, and survivin were determined by Western blot analysis and their mRNA expressions by reverse transcriptase-polymerase chain reaction (RT-PCR). Results: Curcumin significantly induced the growth inhibition and apoptosis of HT-29 cells. A decrease in expressions of Bcl-2, Bcl-xL and survivin was observed after exposure to 10～80 μmol/L curcumin, while the levels of Bax and Bad increased in the curcumin-treated cells. Curcumin also induced the release of cyto- chrome c, the activation of caspase-3, and the cleavage of PARP in a dose-dependent manner. Conclusion: These data suggest that curcumin induced the HT-29 cell apoptosis possibly via the mitochondria-mediated pathway.

Thermally activated phase transitions in Fe-Ni core-shell nanoparticles

Fe-Ni core-shell nanoparticles are versatile functional materials,and their thermal stabilities are crucial for their performances in operating conditions.In this study,the thermodynamic behaviors of Fe-Ni core-shell nanoparticles are examined under continuous heating.The solid-solid phase transition from body centered cubic(bcc)to face centered cubic(fcc)in the Fe core is identified.The transition is accompanied with the generation of stacking faults around the core-shell interface,which notably lowers the melting points of the Fe-Ni core-shell nanoparticles and causes even worse thermal stability compared with Ni ones.Moreover,the temperature of the structural transformation is shown to be tuned by modifying the Ni shell thickness.Finally,the stress distributions of the core and the shell are also explored.The relevant results could be helpful for the design,preparation,and utilization of Fe-based nanomaterials.