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. Author manuscript; available in PMC: 2013 Nov 22.
Published in final edited form as: Surgery. 2011 Jun 15;150(5):10.1016/j.surg.2011.04.002. doi: 10.1016/j.surg.2011.04.002

Fig 3. Dose response of propofol, dose response of increased pressure and the effect of lower oxygen concentration (100torr pO2) on TNF- α production.

Fig 3

Fig 3

Fig 3

Fig 3

Fig 3

3A) Dose response of propofol on increased pressure stimulated TNF-α production. Microglial cells were pre-treated with intralipid (vehicle control) or propofol (2.5μg/ml-20μg/ml) for 30 minutes and then subjected to ambient or 30mmHg extracellular pressure for 24 hours. Increased extracellular pressure significantly stimulated TNF-α secretion in the vehicle control (intralipid) group as well as in cells pretreated with 2.5μg/ml propofol ((* p<0.05, n=6). Propofol at 5.0 μg/ml attenuated the pressure effect (p=0.07, n=6). The higher dose of (10 and 20μg/ml) propofol completely blocked the pressure effect.

3B). Dose response of increased pressure on the TNF-α production and propofol block the pressure effect. Microglial cells were pre-treated with intralipid (vehicle control) or propofol (10μg/ml) for 30 minutes then subjected to ambient or 15 (B-I) or 30mmHg 9B-II) extracellular pressure for 24 hours as described under “Materials and Method”. Increased extracellular pressures at both 15 and 30mmHg significantly stimulated TNF-α secretion in vehicle control (intralipid) groups (*p<0.05, n=6). Propofol completely inhibited the pressure effect.

3C). Propofol block the pressure-induced TNF-α production at lower oxygen concentration (100torr). Microglial cells were pre-treated with intralipid (vehicle control) or propofol (10μg/ml) for 30 minutes then subjected to continuous flow of lower oxygen concentration(~100 torr) or 30mmHg extracellular pressure for 24 hours as described under “Materials and Method”. Increased extracellular pressure at 30mmHg significantly stimulated TNF-α secretion in vehicle control (intralipid) groups (*p<0.05, n=6). Propofol completely inhibited the pressure effect.

3D and E). Effect of increased extracellular pressure on IL-1beta and Il-6 secretion and the role of propofol in the modulation of pressure-induced effect on. Microglial cells were pre-treated with intralipid (vehicle control) or propofol for 30 minutes then subjected to ambient or 30mmHg extracellular pressure for 24 hours as described under “Materials and Method”. Pressure significantly increased IL-1beta but not IL-6 secretion in the vehicle control (intralipid) group (* p<0.05, n=6, D) and the propofol pretreatment group block the pressure-induced IL- 1beta. Similar to vehicle control, propofol also did not alter the Il-6 (p>0.05, n=6, E) secretion in either increased pressure or ambient pressure conditions.