ABSTRACT
Objective To observe the effect of Interferon-α2b on HEL cells (human erythroleukemia cell line) growth, apoptosis and JAK2 V617F mutation gene expression. Methods HEL cells were placed in RPMI1640 containing 10% FBS and incubated in a cell incubator. Cells in the logarithmic growth phasem were collected, adjusting the cell density to 1 × 105/mL for experimental research. The interferon concentration in five groups were 0, 5 × 105, 10 × 105, 50 × 105, 100 × 105 U/L, with different incubation time (0, 24, 72, 120 h), respectively. The cell growth status in different groups was observed in the inverted optical microscope; MTT was used to detect the inhibition of interferon on HEL cell proliferation. Cell apoptosis was detected by flow cytometry. Fluorescence quantitative PCR was used to detect the mutation gene of JAK2 V617F expression. Results Inhibition rates of Interferon on the HEL cell proliferation in 5 × 105 U/L, 10 × 105 U/L, 50 × 105 U/L, 100 × 105 U/L groups were 18.57%, 25.10%, 42.10%, 57.00%, respectively. JAK2 V617F/GAPDH by fluorescence quantitative was 1.556, 1.213, 0.870 respectively under the concentration of interferon 100 × 105 U/L for 24, 72, 120 h. Conclusions Interferon-α2b can inhibit HEL cells proliferation and induce HEL cells apoptosis. Increasing concentration of interferon increases HEL cell apoptosis rate. Interferon can inhibit JAK2 V617F expression of HEL cells in a dose-dependent manner.
ABSTRACT
Objective:This study aimed to achieve the early diagnosis and active treatment of adult hemophagocytic syndrome (HPS) and investigate the clinical characteristics and prognostic factors of this syndrome. Methods:A single-center retrospective analysis was performed to analyze clinical characteristics, laboratory findings, and survival data. Results:In 58 patients, the most common clinical manifestations were fever (100%) and splenomegaly (89.7%). The most common laboratory parameters were serum ferritin 500 g/L (100%) and peripheral cytopenia in two or more lineages (96.6%). platelet count, fibrinogen, and lactate dehydrogenase in the death group were significantly lower than in the survival group (P=0.000, 0.001, and 0.000). Survival analysis results showed that infections in the rheu-matological group exhibited good prognosis [the overall survival (OS) time was not reached in 190 d]. Patients with unexplained causes had moderate prognosis (OS time was 60 d);tumor-associated HPS patients had poor prognosis (the OS time was only 30 d). Univariate analysis results showed that patients with Fbg<1.5 g/L, PLT<40×109/L, and LDH≥2000 U/L also exhibited poor prognosis (P=0.000). Multivariate analysis results showed that PLT<40 × 109/L was an independent adverse factor (HR=6.472, 95%CI:1.526-26.065, P=0.011). Conclusion:HPS exhibits complex clinical manifestations and varied etiology. Patients with infection and rheumatism-related HPS had good prognosiss compared with those manifesting tumor-associated HPS. Fbg<1.5 g/L, PLT<40×109/L, and LDH≥2 000 U/L were the univariate factors that affected the survival time of patients. PLT<40×109/L is an independent adverse factor. These patients need systemic treatments as early as possible.