ObjectiveTo investigate the neuroprotective effects of pyrroloquinoline quinine (PQQ) on oxygen and glucose deprivation (OGD) in cultured rat neuroblastoma cells Neuro2A and the possible mechanisms involved. MethodsCultured rat neuroblastoma cells Neuro2A were pretreated or not pretreated with increasingly concentrations of PQQ, were exposed to 2 h combined OGD in an anaerobic chamber followed by reoxygenation of 6 h. The results on cellular morphology, cell viability，apoptotic cells, reactive oxygen species (ROS), and glutathione (GSH) were compared between OGD and PQQ group. ResultsPretreatment of PQQ (0.4, 0.8, 1.6, 3.2, 6.4, 12.8 μmol/L) increased the cell viability (P＜0.05) and GSH level, decreased the contents of ROS and the percentage of apoptotic cells in cortical neurons exposure to OGD (P＜0.01). ConclusionPQQ exhibits remarkable protection against hypoxia/reoxygenation injury in Neuro2A cells, which may be associated to the inhibiting the oxidative stress and subsequent apoptosis.

BACKGROUND:Pyrroloquinoline quinone is found to accelerate Schwann cel proliferation and growth factor secretion, but there is no report addressing its role in articular cartilage and chondrocytes.
OBJECTIVE: To investigate the role of pyrroloquinoline quinone in chondrocyte proliferation and interleukin-1β-induced chondrocyte apoptosis in the articular cartilage of knee joints and to verify the protective mechanism involved.
METHODS: Chondrocytes were isolated from New Zealand white rabbits (1 month of age), digested under aseptic conditions, and cultured in DMEM/F12 in the presence of 10% fetal bovine serum to alow for proliferation until passage 2. Adherent chondrocytes were cultured in serum-free DMEM/F12 medium with 0, 6.25, 12.5, 25.0, 50.0 and 100.0 μmol/L pyrroloquinoline quinone, separately. Proliferation activity was determined by MTT at 48 hours of pyrroloquinoline quinone administration. Cel cycle was determined by flow cytometry at 30 hours after pyrroloquinoline quinone administration. Apoptosis was determined by flow cytometry folowing 24 hours of pyrroloquinoline quinone pretreatment and 15 hours of interleukin-1β induction.
RESULTS AND CONCLUSION: Pyrroloquinoline quinone enhanced chondrocyte proliferation activity, increased percentage of S phase and G2/M phase in a dose dependent manner and reached the peak when the concentration of pyrroloquinoline quinone was 12.5-25.0 μmol/L (P< 0.05). Pyrroloquinoline quinone also inhibited interleukin-1β-induced chondrocyte apoptosis in early and late stage, and 25.0 μmol/L pyrroloquinoline quinone had the best effects (P < 0.05). These findings suggest pyrroloquinoline quinone can promote chondrocyte division and proliferation, and protect the cels from interleukin-1β-induced apoptosis.

Objective To investigate the effects of ischemic postconditioning (IP) on interleukin-1β (IL-1β) and tunor necrosis factor-α (TNF-α) expression in focal cerebral ischenia/reperfusion in rats in order to clarify the rnechanism of neuroprotective effect of IP.Methods One hundred and ten healthy adult male Sprague-Dawley rats were randomized into sham operation (n =10),ischemia/reperfusion and IP groups.The latter two groups were redivided into 6-,12-,24-,48- and 72-hour subgroups (n =10 in each subgroup) according to their reperfusion time.A focal cerebral ischemia/reperfusion model was induced by the middle cerebral artery intraluminal suture method.After middle cerebral artery occlusion for 2 hours,reperfusion for 15 seconds was conducted using the IP method,and this was repeated for 3 times.The neurobehavioral scores of the rats were evaluated in each group.The infarct volume was measured with 2,3,5-triphenyltetrazolium chloride staining.The expression of TNF-α and IL-1β protein in brain tissue was detected by immunohistochemistry assay.The expression of IL-1β and TNF-αmRNA was determined by in situ hybridization.Results Compared with the ischemia/reperfusion group,the neurobehavioral score and and cerebral infarct volume in the IP group decreased significantly (all P ＜0.05).Expressions of IL-1 β,TNF-o protein and mRNA were slight in the frontoparietal cortex in the sham group; however,they were apparent in ischemia/reperfusion group and IP groups,and began to increase at 6 hours and reached the peak at 24 hours (compared to other time points all P ＜0.05),then decreased gradually.There was the same dynamic change trend in the IP group,and the expression at each time point was significantly lower than that in the ischemia/reperfusion group (all P＜0.05).Conclusions IP significantly down-regulates the expressions of IL-1 β and TNF-α and reduces the infarct volume of the ischemia/reperfusion in rats.These findings indicate that IP may play a neuroprotective role by inhibiting the inflammatory response in brain tissue after ischemia/reperfusion.