Objective To investigate the effect of different doses of propofol on cisplatin-induced hepatotoxicity in rats.Methods Eighty male SD rats weighing 200-250 g,aged 3 months,were randomly divided into 8 groups (n =10 each) ∶ control group (group C),cisplatin 7.5 mg/kg group (group Cis),propofol 180 mg/kg group (group P),intralipid 15 ml/kg group (group Ⅰ),cisplatin 7.5 mg/kg + intralipid 15 ml/kg group (group CisI),cisplatin 7.5 mg/kg + propofol 60 mg/kg group (group CisP1),cisplatin 7.5 mg/kg + propofol 120 mg/kg group (group CisP2),and cisplatin 7.5 mg/kg + propofol 180 mg/kg group (group CisP3).The rats in groups C,Cis,P and I received single intraperitoneal injection of normal saline,cisplatin,propofol and intralipid respectively.While in the groups CisI,CisP1,CisP2 and CisP3,rats received a single intraperitoneal injection of propofol or intralipid at 1 min before a single intraperitoneal injection of cisplatin.At 24 h after cisplatin injection,venous blood samples were taken from inferior vena cava for measurement of plasma ALT and AST activities.The liver tissues were taken for microscopic examination.Results Compared with group C,plasma ALT and AST activities were significantly increased and pathological injury was aggravated in groups Cis,CisI and CisP1-3 (P ＜ 0.05).The activities of ALT and AST were gradually decreased and the pathologic injury was attenuated in groups Cis and CisP1-3 (P ＜ 0.05).Conclusion Propofol can reduce cisplatin-induced hepatotoxicity in a dose-dependent manner in rats.

Objective To investigate the effect of propofol on the gap junction function of BRL-3A cells and cisplatin-induced toxicity to rat hepatic BRL-3A cells. Methods Rat hepatic BRL-3A cell line was provided by professor Tao laboratory of department of pharmacology of our university and cultured in DMEM liquid culture medium at 37℃. The cells were randomly divided into 6 groups: group Ⅰ control (group C) ; group Ⅱ was exposed to intralipid (the solvent) 10 μg/ml (group Ⅰ) ; group Ⅲ was exposed to oleamide (gap junction function inhibitor) 25 μmol/L (group O) and group Ⅳ ,Ⅴ , Ⅵ were exposed to propofol l.5, 2.8 and 4.1 μg/ml respectively (groups P1, 2,3) . Using parachute dye-coupling assay, the dye spread rate and inhibition rate were calculated to measure the gap junction function of BRL-3 A cells. BRL-3 A cells were seeded in two different densities:high density group (seeding density = 1×105 /ml) and low density group (seeding density = 500/ml). Both groups were further divided into 5 subgroups: subgroup Ⅰ control; subgroup Ⅱ was exposed to cisplatin 2.5 μmol/L and subgroup Ⅲ ,Ⅳ ,Ⅴ were exposed to cisplatin 2.5 μmol/L + intralipid 10 μg/ml or oleamide 25 μmol/L or propofol 2.8 μg/ml respectively. The effect of propofol on the cytotoxicity of cisplatin was evaluated by standard colony-forming assay. Results The dye spread rate was significantly lower and inhibition rate higher in groups O,P1 , P2 and P3 than in group C. Propofol decreased the dye spread rate and increased inhibition rate in a concentration-dependent manner. Propofol and oleamide significantly increased colony formation rate in high density group,but had no significant effect on colony formation rate in low density group. Conclusion Propofol can inhibit the gap junction function of BRL-3A cells in a concentration-dependent manner and reduce cisplatin-induced cytotoxicity by inhibiting gap junction function.

Objective To evaluate the effect of propofol on docetaxel-induced toxicity to cervical cancer Hela cells transfected with Cx32 plasmid.Methods Cervical cancer Hela cells transfected with Cx32 plasmid were seeded at two different densities and induced to express Cx32 by incubation with doxycycline for 48 h.The cells at high density were seeded at 1 × 105 cells/ml such that the cells would be confluent at the time of docetaxel exposure.The cells at low density were seeded at 500 cells/ml and the cells did not attach at the density.Each type of cells obtained was randomly divided into 5 groups (n =8 each):control group (group C),docetaxel group (group D),docetaxel + intralipid group (group D + I),docetaxel + 18-α-GA group (D + 18-α-GA),and docetaxel +propofol group (group D + P).Groups D,D + I,D + 18-α-GA and D + P were exposed to 5 nmol/L docetaxel,5 nmol/L docetaxel + 10μg/ml intralipid,5 nmol/L docetaxel + 10 μmol/L 18-α-GA,and 5 nmol/L docetaxel +2.8 μg/ml propofol,respectively.18-α-GA,intralipid and propofol were added prior to docetaxel,and the action time for 18-α-GA alone was 1 h and for intralipid or propofol alone 2 h.The time for coaction between the three drugs and docetaxel was 2 h.Cell survival was determined by a standard colony-forming assay.Results The colony formation rate of the cells seeded at high density in group D was significantly lower than that of the cells seeded at low density in group D (P ＜ 0.05).For the cells seeded at high density,the colony formation rate was significantly decreased in the other groups when compared with group C (P ＜ 0.05).The colony formation rate was significantly higher in groups D + 18-α-GA and D + P than in groups D and D + I (P ＜ 0.05).There was no significant difference in the colony formation rate between groups D and D + I (P ＞ 0.05).For the cells seeded at low density,the colony formation rate was significantly decreased in the other groups when compared with group C (P ＜ 0.05) and there was no significant difference in the colony formation rate between D,D + I,D + 18-α-GA and D + P groups (P ＞ 0.05).Conclusion Propofol can attenuate docetaxel-induced toxicity to Hela cells transfected with Cx32 plasmid and inhibition of gap junction function is involved in the mechanism.

BACKGROUND:For depressed skul fractures in children, retaining their skul and narrowing surgical incision meet the concept of minimaly invasive surgery as important as ensuring the surgical safety and therapeutic effects, which is also the requirement of children’s parents. OBJECTIVE:To explore the curative effects of in suit replantation of free bone fragments based on a smal incision in children with depressed skul fractures. METHODS: Fifteen patients with depressed skul fractures, aged 3-16 years, were selected and subject to CT examination and manual examination of the scalp at fractured site under general anesthesia for labeling fracture range. Then, one or two bone fragments corresponding to the fracture site and size were selected. A smal incision with a length equal to the outer edge of bone fragments removed. Postoperative folow-up was employed for observation of clinical effects. RESULTS AND CONCLUSION:An incision, 5-7 cm in length, were made, and one bone fragment was removed from six cases, and two bone fractures were removed from nine cases. Intraoperatively, there were six cases of epidural hematoma, three cases of subdural hematoma, six cases of brain contusion and bleeding. For fracture fixation, one skul lock was used in eight cases, two skul locks in six cases, and three bone plates in one cases. Postoperative CT showed 12 cases of good fracture reduction displayed basic symmetry with the contralateral skul; 3 cases showed partialy depressed bone fragments that were less than 0.5 cm; 6 cases had a little skul defects with a diameter < 1.0 cm; 6 cases had mild epidural hematoma or effusion which was eliminated after conservative treatment. Eleven of 15 cases were folowed for 2 month to 3 years, and showed no changes in skul shape on CT films compared with those at discharge and presented with good stability. In addition, there were one case of mild limb paralysis, one case of mild language barriers, and one case of mild seizures, but al these cased were wel controled by drugs. These findings indicate that in situ replantation of partialy free bone fragments is suitable for depressed skul fractures in children.