[Molecular mechanism underlying the inhibitory effect of propofol on lipopolysaccharide-induced pyroptosis of mouse bone marrow-derived macrophages].

OBJECTIVE: To investigate the molecular mechanism underlying the inhibitory effect of propofol on pyroptosis of macrophages. METHODS: Macrophages derived from bone marrow were extracted and divided into three groups: control group, LPS+ATP group and propofol+LPS+ATP group. The control group was not given any treatment; LPS+ATP group was given LPS 1 µg/mL stimulation for 4 h, then ATP 4 mM stimulation for 1 h; Propofol+LPS+ATP group was given propofol+LPS 1 µg/mL stimulation for 4 h, then ATP stimulation for 1 h. After treatment, the supernatant and cells of cell culture were collected. the cell activity was detected by CCK8 and flow cytometry. The inflammatory cytokines IL-1ßand IL-18 were detected by Elisa. Western blot was used to detect the expression of caspase-1 protein and TLR4 on cell membran Immunohistochemical fluorescence was used to detect apoptosis of cells. RESULTS: LPS+ATP significantly decreased the viability of the macrophages and increased the cellular production of IL-1ß and IL-18, activation of caspase-1 protein and the expression of TLR-4 on the cell membrane (P < 0.05). Treatment with propofol obviously reversed the changes induced by LPS+ATP. CONCLUSIONS: LPS+ATP can induce pyroptosis of mouse bone marrow-derived macrophages, and propofol effectively inhibits such cell death, suggesting that propofol anesthesia is beneficial during operation and helps to regulate the immune function of in patients with sepsis.

[Application of dexmedetomidine combined with propofol in patients undergoing painless colonoscopy for colonic polyps resection under Narcotrend monitoring].

OBJECTIVE: This clinical study was conducted to investigate the effects of dexmedetomidine (DEX) combined with propofol on vital signs and anaesthetic depth in patients. METHODS: Ninety patients with ASA 1-2 requiring painless colonoscopy for colonic polyps resection were randomized to receive DEX 0.3 micro;g/kg (group D, n=45) followed by propofol 1 mg/kg or propofol 2 mg/kg (group C, n=45), and according to the body activity and operation time, additional doses of propofol (0.2-0.5 mg/kg) were given. The full recovery time, operation time, consumed dose of propofol, mean arterial pressure (MAP), heart rate (HR), hemoglobin oxygen saturation levels(SPO2) and NTI were recorded. RESULTS: The SPO2recover time and the consumed dose of propofol in group D were decreased compared to those in group C (P<0.01). The rate of the body activity in group D was lower than that in group C (P<0.05). The NTI in group C was lower than that in group D (P<0.05). The HR and MAP were similar in both groups. CONCLUSION: Under Narcotrend monitoring, the value of DEX combined with low dose of propofol in colonoscopy for colonic polyps resection is to reach more reasonable depth of anesthesia to reduce adverse responses and the dose of propofol.

Inhibition of S100A9 expression by propofol in monocytes of rats with endotoxemia.

The inflammatory response is a non-specific autoimmune response. Monocytes are the most important effector cells in the systemic inflammatory response. In recent years, the function of the intravenous anesthetic, propofol, in the inhibition of the inflammatory response has attracted much attention. However, the specific signal transduction mechanism related to the anti-inflammatory effect of propofol remains unclear. In this study, monocyte protein expression in rats with endotoxemia was detected using proteomic techniques before and after propofol intervention. By two-dimensional electrophoresis and mass spectrometric identification, we found that S100A9 protein expression was significantly reduced after propofol treatment. In addition, we used western blot analysis to confirm the results of two-dimensional electrophoresis. The S100A9 protein, a member of the S100A calcium-binding protein family, is closely related to the occurrence and development of inflammation. The results of this study suggest that the anti-inflammatory effect of propofol may be related to the inhibition of S100A9 protein expression.

[Analgesic effect of COX inhibitors and its mechanism in a rat model of neuropathic pain].

OBJECTIVE: To investigate the effect of COX inhibitors on pain threshold and spinal N-methyl-D-aspartate (NMDA) receptor subunit 2B (NR2B) expression in a rat model of neuropathic pain. METHODS: Thirty-six male SD rats were randomly divided into sham-operated group, chronic constriction injury (CCI) of the sciatic nerve group, indomethacin+CCI group, and parecoxib+CCI group with corresponding treatments. All the rats were tested for mechanical withdrawal threshold, and at day 13 after the surgery, the rats were decapitated for detection of NR2B expression in the spinal cord at the L4-6 levels. RESULTS: The mechanical withdrawal threshold were lowered significantly after the operation in CCI, indomethacin+CCI and parecoxib+CCI groups (P<0.05). Parecoxib alleviated the hypersensitivity of CCI model rats but not affected spinal NR2B expressions (P>0.05). No significant differences were found in the mechanical withdrawal threshold or spinal NR2B expression between CCI group and indomethacin+CCI group (P>0.05). CONCLUSION: Parecoxib can alleviate neuropathic hypersensitivity in rats, but this effect may not be associated with NR2B expression in the spinal cord.

[Effect of electroacupuncture on pain threshold and spinal NR2B subunit expression in a rat model of neuropathic pain].

OBJECTIVE: To observe the effect of electroacupuncture (EA) on pain threshold and spinal NR2B subunit expression in a rat model of neuropathic pain due to chronic compression injury (CCI) of the sciatic nerve and explore the analgesic mechanism of EA. METHODS: Male SD rats weighing 200-280 g were randomly divided into 4 groups (n=10), namely the sham-operated group, CCI group, EA+CCI group, and sham EA+CCI group. All the rats underwent tests of the mechanical withdrawal threshold and thermal threshold. On day 13 after the surgery, all the rats were decapitated to collect the L4-6 segments of the spinal cord to examine NR2B expression using Western blotting. RESULTS: The postoperative mechanical withdrawal threshold and thermal threshold were significantly lowered in CCI, EA+CCI and sham EA+CCI groups as compared to those before the surgery (P<0.05). EA obviously alleviated the hypersensitivity in the rats with CCI and inhibited spinal NR2B expressions (P<0.05). No significant differences were found in the mechanical withdrawal threshold, thermal threshold or spinal NR2B subunit expression between CCI group and sham EA+CCI group (P>0.05). CONCLUSION: EA may alleviate neuropathic hypersensitivity partially by inhibiting NR2B expression in the spinal cord of rats with neuropathic pain resulting from CCI of the sciatic nerve.