Recent advances in the role of SIRT3 in leukemia drug resistance / 上海交通大学学报（医学版）

Leukemia is a clonal malignant disease originating from abnormal hematopoietic stem cells or progenitor cells. The key issue of leukemia treatment is its drug-resistance. SIRT3 is the main mitochondrial NAD+ dependent deacetylase. It regulates enzymes and transcription factors of many metabolism pathways. SIRT3 acts both as oncogenic gene and tumor-suppressing gene in the oncogenesis of different cancers. Studies have shown that reactive oxygen species (ROS) level is closely related to drug resistance of cancer cells. ROS level is elevated in leukemia cells, thus affecting its drug resistance. SIRT3 can downregulate ROS level in many ways and enhance cell survival in the case of oxidative stress. Decreased deacetylase activity of SIRT3 makes leukemic cells more vulnerable to oxidative stress so that they are more sensitive to current chemotherapies. Through discovering the function of SIRT3 in leukemia cells, a chance of finding a new target for leukemia treatment can be found. This article reviews recent advances on the role of SIRT3 in leukemia drug resistance.

Investigation of metabolites of Triptergium wilfordii on liver toxicity by LC-MS / 中国中药杂志

In this paper, biomarkers of liver toxicity of Triptergium wilfordii based on metabolomics was screened, and mechanism of liver toxicity was explored to provide a reference for the clinical diagnosis for liver toxicity of Triptergium wilfordii. MS method was carried on the analysis to metabolic fingerprint spectrum between treatment group and control group. The potential biomarkers were compared and screened using the multivariate statistical methods. As well, metabolic pathway would be detailed description. Combined with PCA and OPLS-DA pattern recognition analysis, 20 metabolites were selected which showed large differences between model group and blank group (VIP > 1.0). Seven possible endogenous biomarkers were analyzed and identified. They were 6-phosphate glucosamine, lysophospholipid, tryptophan, guanidine acetic acid, 3-indole propionic acid, cortisone, and ubiquinone. The level changes of above metabolites indicated that the metabolism pathways of amino acid, glucose, phospholipid and hormone were disordered. It is speculated that liver damage of T. wilfordii may be associated with the abnormal energy metabolism in citric acid cycle, amino acid metabolism in urea cycle, and glucose metabolism. It will be helpful to further research liver toxicity ingredients of Triptergium wilfordii.

Effect of total saponins of Panax notoginseng on transdifferentiation of rats' tubular epithelial cell induced by IL-1alpha / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To study whether total saponins of Panax notoginseng (PNS) can prevent renal interstitial fibrosis occurrence through blocking the IL-1alpha induced tubular epithelial cell and decrease the secretion of extracellular matrix (ECM).</p><p><b>METHODS</b>Normal rats' tubular epithelial cells NRK52E were cultured in vitro, their morphological changes were observed by inverted phase contrast microscope and scanning electron microscope. Flow cytometry technique and immuno-histochemical method was used to detect the expression of alpha-smooth muscle actin (alpha-SMA), and ELISA was used to quantitatively detect the fibronectin (FN) in the supernatant</p><p><b>RESULTS</b>IL-1alpha could induce the transdifferentiation of tubular epithelial myofibroblast, showing hypertrophy of cells elongated and fusiform-shaped, with significantly enhanced expression of alpha-SMA and increased secretion of FN (P<0.05). After adding PNS of different concentrations, the morphology of cells restored close to normal tubular epithelial cells, with the increase of alpha-SMA expression and FN secretion significantly inhibited (P<0.05) in dose-dependent manner (P<0.05). But addition of different dosages of PNS alone showed no effect on tubular cells.</p><p><b>CONCLUSION</b>IL-1alpha could induce the transdifferentiation of tubular epithelial myofibroblast, promote the deposition of ECM component FN. PNS could inhibit IL-1alpha induced the transdifferentiation of NRK52E and secretion of ECM, therefore, PNS could be taken as a new drug for prevention and treatment of renal interstitial fibrosis and terminal stage of renal diseases.</p>