Patients with diabetic peripheral neuropathy experience debilitating pain that significantly affects their quality of life (Abbott et al., 2011), by causing sleeping disorders, anxiety, and depression (Dermanovic Dobrota et al., 2014). The primary clinical manifestation of painful diabetic neuropathy (PDN) is mechanical hypersensitivity, also known as mechanical allodynia (MA) (Callaghan et al., 2012). MA's underlying mechanism remains poorly understood, and so far, based on symptomatic treatment, it has no effective therapy (Moore et al., 2014).
Animals ; CX3C Chemokine Receptor 1/physiology* ; Chemokine CX3CL1/physiology* ; Diabetes Mellitus, Experimental/complications* ; Diabetes Mellitus, Type 1/complications* ; Diabetic Neuropathies/etiology* ; Hyperalgesia/etiology* ; Mice ; Mice, Inbred C57BL ; Spinal Cord/physiology* ; Streptozocin/pharmacology*

OBJECTIVETo observe the changes of human umbilical venous endothelial cells (HUVECs) induced by the sera from children with active Henoch-Sch-nlein purpura (HSP) and the protective effects of methylprednisolone against HUVECs injury.

METHODSHUVECs were divided into four groups based on the culture conditions: blank control group, normal serum group, HSP serum group, and HSP serum plus methylprednisolone group. The levels of tumor necrosis factor (TNF)-α and interleukin (IL)-8 in the supernatants of each group were detected using ELISA and the nitric oxide (NO) level by nitrate reductase determination. Moreover, the expressions of nuclear factor-kappa B (NF-κB) and Fractalkine in HUVECs were examined by semiquantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blot, respectively.

RESULTSThe levels of IL-8, TNF-α, and NO in the HSP serum group were significantly higher than those in the blank control and normal serum groups (P<0.05). Compared with the HSP serum group, the levels of IL-8, TNF-α, and NO in the HSP serum plus methylprednisolone group decreased significantly (P<0.05). The mRNA expression levels of NF-κB and Fractalkine in the HSP serum group were significantly higher than those in the blank control group (P<0.05). The protein expression levels of NF-κB and Fractalkine in the HSP serum group were significantly higher than those in the blank control and normal control group (P<0.05). Compared with the HSP serum group, the mRNA and protein expression levels of NF-κB and Fractalkine in the HSP serum plus methylprednisolone group decreased significantly (P<0.05).

CONCLUSIONSThe sera from children with active HSP can induce the in vitro cultured HUVECs to become activated and excrete cytokines. Methylprednisolone may inhibit NF-κB expression, reduce the production of inflammatory factors, and thus alleviate vascular inflamation.

Cells, Cultured ; Chemokine CX3CL1 ; analysis ; genetics ; Child ; Child, Preschool ; Cytokines ; blood ; Cytoprotection ; Female ; Human Umbilical Vein Endothelial Cells ; drug effects ; immunology ; metabolism ; Humans ; Male ; Methylprednisolone ; pharmacology ; NF-kappa B ; analysis ; antagonists & inhibitors ; genetics ; Nitric Oxide ; physiology ; Purpura, Schoenlein-Henoch ; blood