ABSTRACT
Objective To investigate the protective effect of molecular hydrogen against hydrogen peroxide (H2O2)-induced oxidative injury in primary cultures of rat spinal cord neurons and the related mechanism. Methods Rat spinal cord neurons were cultured for 7 days and were randomly assigned to four groups with different treatments-(1) Normal medium (NM) control: treated with NM; (2) Hydrogen-rich medium(HM): treated with HM; (3) NM+H2O2: treated with 100 μmol/L H2O2 and 15 μmol/L ferrous chloride (FeCl2) after pretreatment with NM for 2 h; and (4) HM+H2O2: treated with 100 μmol/L H2O2 and 15 μmol/L FeCl2 after pretreatment with HM for 2 h. The respective media were changed every 6 h in each group, and 12 h later the cells were collected for assays of reactive oxygen species (ROS), hydroxyl radical (HO •), apoptosis, and the expression of glycogen synthase kinase-3β (GSK-3β) and p-GSK-β. Results Compared with NM, HM significantly reduced the H2O2-induced intracellular production of ROS and HO • in purified neurons (P<0. 01), significantly decreased the number of apoptotic neurons (P < 0. 01) and expression of caspase-3 (P < 0. 01), and significantly promoted phosphorylation of GSK-β (P<0. 01). Conclusion Molecular hydrogen has protective effect against H2O2-induced oxidative injury in primary cultured neurons. Themechanisms might be related to reduction of intracellular production of ROS and HO •, inhibition of apoptosis in neurons and promotion of GSK-β phosphorylation.
ABSTRACT
The mechanism of neuropathic pain is extremely complex. Despite of great research efforts on the pathogenesis of neuropathic pain and development of new drugs in recent years, the mechanism of neuropathic pain remains unclear. CCL5 belongs to the C-C chemokine subfamily, and its abnormal regulation of inflammatory responses under pathological condition may induce or exacerbate a variety of diseases. Recently, many researches have suggested that CCL5 has the potential of mediating neuropathic pain, but with unknown mechanism. This paper reviewed the role of CCL5 in the development and regulation of neuropathic pain and discussed the possibility of CCL5 as an cause of neuropathic pain.