Effect of methyl eugenol on hypoxia/reoxygenation injury of human renal tubular epithelial cells and its mechanism / 中国中药杂志

This study aimed to investigate the effect of methyl eugenol(ME) on hypoxia/reoxygenation(H/R)-induced injury of human renal tubular epithelial HK-2 cells and its mechanism. The viability of HK-2 cells cultured with different concentrations of ME and exposed to H/R was detected by cell counting kit-8(CCK-8) assay. The effect of ME on the morphology of HK-2 cells was observed under an inverted microscope. The content of intracellular reactive oxygen species in different groups was detected after 2',7'-dichlorodihydrofluorescein diacetate(DCFH-DA) fluorescence staining. Cell apoptosis was determined by flow cytometry. Changes in mitochondrial membrane potential were monitored by JC-1 dye. The concentrations of nuclear factor erythroid 2 related factor 2(Nrf2), heme oxygenase-1(HO-1), and nicotinamide adenine dinucleotide phosphatase oxidase 4(Nox4) were measured by Western blot, followed by the assay of Nrf2 concentration changes in cytoplasm and nucleus by confocal fluorescence staining. The results showed that when the concentration of ME was 0-40 μmol·L~(-1), the activity of HK-2 cells was not affected. Compared with the model group, ME enhanced the activity of HK-2 cells and the cell morphology was normal. As revealed by further experiments, ME inhibited the release of reactive oxygen species and the decline in mitochondrial membrane potential of HK-2 cells after H/R injury, promoted Nrf2/HO-1 expression and Nrf2 translocation to the nucleus, and down-regulated the expression of Nox4, thereby significantly reducing apoptosis. This protective effect of ME could be reversed by the specific Nrf2 inhibitor ML385. These findings have preliminarily proved that ME effectively protected HK-2 cells against H/R injury, which might be related to its promotion of Nrf2/HO-1 signaling pathway and inhibition of Nox4. Such exploration on the possible mechanism of ME in the treatment of renal ischemia-reperfusion injury(IRI) and protection of organ function from the perspective of antioxidant stress has provided reference for related research on the treatment of acute kidney injury with traditional Chinese medicine.

Clinical assessment of preventing febrile nonhemolytic transfusion reaction by leukocyte-depleted blood transfusion / 中国实验血液学杂志

The objective was designed to assess the clinical efficiency of preventing febrile nonhemolytic transfusion reactions (FNHTR) with transfusion of leukocyte-depleted RBC and platelet concentrates. One hundred patients with cirrhosis of liver, gastric ulcer and cancer were selected to receive RBC concentrates with leukocyte filtration. Another group of 50 patients with liver necrosis, gastric ulcer and cancer were selected to receive non-filtered RBC concentrates. Two hundred and forty patients with acute or chronic leukemia, aplastic anemia, multiple myeloma, thrombocytopenia purpura, diabetes mellitus, cirrhosis of liver, upper gastrointestinal hemorrhage, severe hepatitis, burn and cancer post radioactive or chemical treatment were divided into two group with 120 patients in each one and selected randomly to receive platelet concentrates. The incidence rates of FNHTR in all patients were investigated. Results showed that there was no FNHTR in 100 transfusions with leukocyte-depleted RBC concentrates. Eight out of 50 patients with non-filtrated RBC concentrates showed FNHTR. The incidence of FNHTR was sixteen (16%) in non-filtrated transfusion. Twenty-five and 7 patients manifested FNHTR respectively in non-filtrated or filtrated platelets transfusions. The incidence of FNHTR was 20.83% and 5.83% respectively in non-filtrated or filtrated platelet transfusion. It is concluded that leukocyte-depleted RBC and platelet concentrates reduces FNH TR in blood transfusion.