Objective To observe the inhibitory effect of pyridoxine hydrochloride (PN) combined with common chemotherapeutics on mice hepatoma cells H22 in vitro. Methods MTT assay was used to determine the effects of PN in combination with 10 different antineoplastic agents on H22 cells, and immuno-histochemistry was used to observe the distribution of PN in H22 cells and morphologic changes of the cells before and after PN treatment. Results After 24 hours incubation with 5 mmol/L PN, the treated cells expanded apparently with nucleus chipping. PN entered the tumor cell and was mainly condensed in cytoplasma and H22 cells were sensitive to PN. When administered concomitantly with chemotherapic agents, most of the combinations showed antagonistic effects while a few of the combinations were additive. For instance, doxorubicin (ADM) used in combination with PN inhibited cell proliferation with an IR value (IR=0.63) much lower than ADM alone (IR=0.71, P<0.01), and the CI value was less than 0.9, which indicated an antagonistic effect. However, PN in combination with ifosfamide (ICTX) showed additive effect (CI>0.9), and the IR value (IR=0.60) in combined group was higher than that (IR=0.40) in ICTX group (P<0.05). Conclusion PN treatment could increase the intracellular PLP level and result in growth inhibition and cell death, and combined administration of PN and ICTX might be a potential method to improve efficacy and to reduce toxic effects while a co-administration of PN and ADM should be avoided.

Objective: To investigate the protective effect of propofol on neurological function in rats after traumatic brain injury (TBI) and its possible mechanism. Methods: A total of 96 SD rats were randomly divided into sham operation group, sham operation+ propofol group, TBI group and TBI + propofol group, with 24 rats in each group. The TBI model was prepared by modified Feeney method. The sham operation+ propofol group and the TBI+ propofol group were given 50 mg/kg of propofol once daily. The sham operation group and the TBI group were injected with the same amount of normal saline. Modified neurobehavioral functional scores (mNSS) were evaluated at 1, 3, 7 and 14 days after injury; dry-wet specific gravity method was used to detect brain water content in injured area; TUNEL staining was used to detect neuronal apoptosis; chemiluminescence was used to detect activity of Oxygen cluster (ROS) content; Western blot was used to determine the expressions of inositol requirement enzyme 1 (IRE-1), enhancer binding protein homolog protein (CHOP), heme oxygenase 1 (HO-1), quinone oxidoreductase 1 (NQO1) and nuclear factor E2 related factor 2 (Nrf2) protein. Results: Compared with the sham operation group and the sham operation + propofol group, the mNSS, brain tissue water content, apoptosis number and ROS increased at 1, 3, 7 and 14 days after TBI in the TBI group and TBI + propofol group (P<0.05). Compared with TBI group, mNSS in TBI+ propofol group decreased significantly [(9.3±1.4)points ∶(10.9±1.2)points] 7 days after injury (P<0.05); the brain tissue water content decreased significantly [(81.0±0.8)%∶(82.1±0.8)%] 3 days after injury (P<0.05); the number of apoptotic cells decreased significantly 7 days after injury[(14.1±1.4)%∶(15.6±1.6)%], with the most significant decrease at 14 days after injury [( 10.4±1.5)%∶(13.2±1.4)% (P<0.05); and ROS decreased significantly 7 days after injury [(61.5±4.0)RFU∶(77.3±5.5)RFU](P<0.05). Compared with the sham operation group and the sham operation+ propofol group, the expressions of IRE-1 and CHOP were significantly up-regulated in the TBI group and the TBI+ propofol group (P<0.05); the expressions of HO-1, NQO1 and Nrf2 in the TBI group were significantly decreased (P<0.05); the expressions of HO-1 and NQO1 in TBI+ propofol group were increased (P<0.05) while the expression of Nrf2 were decreased slightly (P<0.05). Compared with the TBI group, the expressions of IRE-1 and CHOP in TBI+ propofol group were decreased (P<0.05), while the expressions of HO-1, NQO1 and Nrf2 were significantly increased (P<0.05). Conclusion After TBI in rats, propofol can reduce oxidative stress by activating the Nrf2-antioxidant element (ARE) pathway, reduce brain edema, and inhibit neuronal apoptosis, thus playing a neuro-protective role.