Polysaccharides from Lentinus edodes and Tricholoma matsutake could enhance the efficacy of 5-FU-mediated H22 cell growth inhibition.

Bone marrow mesenchymal stem cells (BMSCs) are potential therapy for diabetes. Owing to the oxidative stress caused by hyperglycemia, these transplanted BMSCs are with high rate of apoptotic death after transplantation. Ginkgo biloba L. extract (EGB) is a potent antioxidant which can remove free radicals. The study was to investigate whether EGB can protect BMSCs from oxidative stress in vitro and enhance the efficacy of BMSCs in lowering blood glucose levels after transplantation. BMSCs were cultured with H2O2, EGB, or H2O2 and EGB. Cell viability, malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and cell death rates were determined. Diabetes was induced by single injection of streptozotocin (STZ) in male Wistar rats. Diabetic rats received EGB, BMSCs, or EGB/BMSCs. The serum levels of glucose, insulin, interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), MDA, SOD, and GSH-Px were determined. PKCα expression and NF-κB activation in kidney were determined. The MDA levels and cell death rates in BMSCs cultured with H2O2 and EGB were significantly lower; cell viability, SOD, and GSH-Px activities were significantly higher compared with those with H2O2 alone. Compared with diabetic rats receiving BMSCs, diabetic rats receiving EGB before BMSCs transplantation showed (1) significantly lower levels of blood glucose, serum MDA, IL-6, and TNF-α, and higher levels of insulin, SOD, and GSH-Px activities; (2) significantly lower PKCα expression and NF-κB activation in the kidney. EGB administration before BMSC transplantation can enhance the effectiveness of BMSCs in lowering blood glucose levels and reversing oxidative stress in diabetic rats.

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These authors contributed equally to this workPurpose: To evaluate the expression in human clear cell renal cell carcinoma (ccRCC) tissues and explore the effects of kinesin family member 4A (KIF4A) on ccRCC progression. Methods: GEPIA was used to evaluate the mRNA levels of KIF4A in human ccRCC tissues from TCGA database, and Immunohistochemistry (IHC) assays were performed to assess its expression in human ccRCC tissues collected in our hospital. The clinical-pathological analysis was performed to explore the correlation with KIF4A expression. The effects of KIF4A on ccRCC cell proliferation were detected through colony formation and MTT assays. Finally, the effects of KIF4A on tumor growth were measured using a mice model. Results: Bioinformation results showed the expression of KIF4A mRNA was upregulated in ccRCC tissues and high expression of KIF4A was related with poor prognosis in ccRCC patients. We also found a high expression of KIF4A in human ccRCC tissues collected in our hospital. We also found its expression level was correlated with clinical characteristics, including T stage (P=0.035*) and lymphatic metastasis (P=0.028*). We further confirmed that knockdown of KIF4A suppressed cell proliferation in HTB-47 and CRL-1932 cells. Furthermore, KIF4A contributes to tumor growth of ccRCC cells in mice. Conclusion: We found the abnormal high expression of KIF4A in human ccRCC tissues and demonstrated that KIF4A could serve as a tumor induction gene.

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