Mohamed Zaki

Human mesenchymal stem cells (hMSCs) are mostly studied for their potential clinicaluse. Little is known about the underlying molecular mechanisms that link hMSCs to the targeted inhibition of tumor cells. The present study was conducted to evaluate the tumor suppressive effects of human mesenchymal stem cells (hMSCs) on human hepatoma cell line (HepG2) and their signaling mechanisms.

Human mesenchymal stem cells (hMSCs) are mostly studied for their potential clinical use. Little is known about the underlying molecular mechanisms that link hMSCs to the targeted inhibition of tumor cells. The present study was conducted to evaluate the tumor suppressive effects of human mesenchymal stem cells (hMSCs) on human hepatoma cell line (HepG2) and their signaling mechanisms. To fulfill this objective, the influence of hMSCs on genes concerned with apoptosis, mitogenesis as well as on the proliferation of HepG2 cell line was investigated using either hMSCs-conditioned or using hMSCs and HepG2 co-culture conditioned media. Cell survival was evaluated using cell proliferation (MTT) assay kit. Gene expression of survivin, proliferating cell nuclear antigen (PCNA), β-Catenin, telomerase and VEGF was assessed by real time reverse transcription-polymerase chain reaction (RT-PCR). HpG2 cells cultured with either hMSCs-conditioned media or with hMSCs&HepG2 co-culture conditioned media showed decreased proliferation and decreased expression of survivin, PCNA, β-Catenin and telomerase. However, both media had increased expression of VEGF. Treatment of HepG2 cells by either hMSCs conditioned media or by hMSCs and HepG2 co-culture condition media led to a significant decrease in cell proliferation and down regulation of genes concerned with antiapoptosis, mitogenesis, and cell proliferation. This indicates that hMSCs can suppress tumorigenesis through factors produced in their conditioned media.

The toxic effect of Pb ion (lead acetate) was investigated using male albino rats, which was ingested at 1/20, 1/40, and 1/60 sublethal doses. Relative to normal control, the ingestion of Pb2+ induced significant stimulation in ALT and AST activity. In addition, total soluble protein and albumin contents of plasma were decreased, while the content of globulin was changed by the Pb2+ treatments. The cholinesterase activity was inhibited, but the activities of alkaline and acid phosphates as well as lactate dehydrogenase were stimulated as a result of lead acetate intoxication. These observations were gradually paralleled across the experiment dose of the three doses of intoxicated Pb2+. In the case of blood picture, Pb2+ ingestion significantly reduced the contents of hemoglobin and RBC count of intoxicated rat’s blood, while the plasma levels of T3 and T4 and blood WBC count were insignificantly decreased or unchanged. All results of the present study showed that the Pb2+ ingestion was more effective in the case of the high dose (1/20 LD50) than that of the low dose (1/60 LD50) ingestion relative to the normal healthy control. The results of the present work advice the need to avoid exposure of humans to the lead compound to avoid injurious hazard risk.

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