Objective: To explore the modulating effect of endogenous sulfur dioxide (SO2) on the ba-lance of oxidation/reduction in the cecal-ligation-and-puncture-induced septic rat myocardium.
Methods: Forty male Sprague Dawley rats were randomized into control group, SO2group, sepsis group and sepsis + SO2group. The levels of procalcitonin (PCT), creatine kinase isoenzyme (CK-MB), cardiac troponin Ⅰ (cTn Ⅰ) and fatty acid binding protein (FABP) in plasma in each group of the rats were measured; The level of hydrogen peroxide (H2O2), level of nitric oxide (NO), activity of myeloperoxidase (MPO), activity of hydroxyl free radical (·OH) and level of malondialdehyde (MDA) in myocardial tissue were measured; Total antioxidant capacity (T-AOC), activity of catalase (CAT), level of cytochrome oxidase (CO), level of glutathione (GSH), level of glutathione oxidase (GSH-px) and activity of superoxide dismutase (SOD) in myocardial tissue were measured.
Results: The level of PCT in plasma in the rats with sepsis increased from (0.93±0.26) μg/L to (2.45±0.52) μg/L (P < 0.01), and decreased to (1.58±0.36) μg/L after the intervention of sulfur dioxide donor (P < 0.01). In sepsis, the plasma CK-MB, cTn Ⅰ and FABP levels in the rats increased respectively from (14.46±6.48) μg/L, (151.25±30.14) ng/L and (2.72±0.65) μg/L to (23.72±7.72) μg/L, (272.78±52.70) ng/L and (5.22±1.01) μg/L (P all < 0.01), and decreased to (16.74±3.63) μg/L, (184.86±37.72) μg/L and (3.31±0.84) μg/L (all P < 0.05) after the intervention of sulfur dioxide donor. The level of H2O2, level of NO, activity of MPO, activity of ·OH and level of MDA in myocardial tissue in the rats with sepsis increased respectively from (67.26±8.77) mmol/g, (38.39±6.93) μmol/g, (358.25±68.12) U/g, (648.42±93.69) U/ mg and (4.55±0.96) μmol/g to (111.45±17.35) mmol/g, (51.04±5.91) μmol/g, (465.88±76.76) U/g, (873.75±123.47) U/mg and (7.25±0.86) μmol/g (all P < 0.01), and decreased respectively to (75.99±10.52) mmol/g, (39.39±7.80) μmol/g, (393.17±51.5) U/g, (710.54±106.33) U/mg and (5.16±0.65) μmol/g after the intervention of the sulfur dioxide donor (all P < 0.05). The activity of T-AOC, activity of CAT, level of CO, level of GSH, level of GSH-px and activity of SOD in myocardial tissue in the rats with sepsis increased respectively from (2.07±0.37) U/mg, (169.25±36.86) U/g, (1.35±0.32) μmol/g, (103.51±16.62) μmol/g, (38.40±7.97) μmol/g and (38.50±8.30) U/mg to (1.42±0.39) U/mg, (98.44±26.56) U/g, (0.96±0.21) μmol/g, (68.05±7.35) μmol/ g, (23.83±5.04) μmol/g and (23.11±4.63) U/mg (P all < 0.01), and increased respectively to (1.83±0.37) U/mg, (146.14±31.63) U/g, (1.28±0.20) μmol/g, (92.10±11.84) μmol/g, (37.16±3.01) μmol/g and (37.29±2.62) U/mg (P all < 0.05) after the intervention of the sulfur dioxide donor.
Conclusion: Endogenous SO2 can protect rat myocardium in sepsis by modulating the ba-lance of oxidation and reduction.
目的: 探索内源性二氧化硫对盲肠结扎穿刺术诱导的脓毒症大鼠心肌氧化应激的调节作用。
方法: 雄性Sprague Dawley大鼠40只，随机分入对照组、二氧化硫组、脓毒症组及脓毒症+二氧化硫组。检测各组大鼠血浆降钙素原(procalcitonin，PCT)、肌酸激酶同工酶(creatine kinase isoenzyme，CK-MB)、肌钙蛋白Ⅰ(cardiac Troponin Ⅰ，cTnⅠ)及脂肪酸结合蛋白(fatty acid binding protein，FABP)含量，检测各组大鼠心肌组织中过氧化氢(hydrogen peroxide，H2O2)含量、一氧化氮(nitric oxide，NO)含量、髓过氧化物酶(myeloperoxidase，MPO)活性、羟自由基(hydroxyl free radical，·OH)活性及丙二醛(malondialdehyde，MDA)含量，检测各组大鼠心肌组织总抗氧化能力(total antioxidant capacity，T-AOC)、过氧化氢酶(catalase，CAT)活性及细胞色素氧化酶(cytochrome oxidase，CO)含量、谷胱甘肽(glutathione，GSH)含量、谷胱甘肽氧化酶(glutathione oxidase，GSH-px)含量及超氧化物歧化酶(superoxide dismutase，SOD)活性。
结果: 脓毒症时大鼠血浆PCT含量由(0.93±0.26) μg/L升高至(2.45±0.52) μg/L(P<0.01), 二氧化硫供体干预后降低至(1.58±0.36) μg/L(P<0.01)。脓毒症时大鼠血浆CK-MB、cTnⅠ及FABP含量分别由(14.46±6.48) μg/L、(151.25±30.14) ng/L及(2.72±0.65) μg/L升高至(23.72±7.72) μg/L、(272.78±52.70) ng/L及(5.22±1.01) μg/L(P均<0.01)，二氧化硫供体干预后分别降低至(16.74±3.63) μg/L、(184.86±37.72 ng/L)及(3.31±0.84) μg/L(P均<0.05)。脓毒症时大鼠心肌组织H2O2含量、NO含量、MPO活性、·OH活性及MDA含量分别由(67.26±8.77) mmol/g、(38.39±6.93) μmol/g、(358.25±68.12) U/g、(648.42±93.69) U/mg及(4.55±0.96) μmol/g升高至(111.45±17.35) mmol/g、(51.04±5.91) μmol/g、(465.88±76.76) U/g、(873.75±123.47) U/mg及(7.25±0.86) μmol/g(P均<0.01)。二氧化硫供体干预后分别降低至(75.99±10.52) mmol/g、(39.39±7.80) μmol/g、(393.17±51.5) U/g、(710.54±106.33) U/mg及(5.16±0.65) μmol/g(P均<0.05)。脓毒症时大鼠心肌组织T-AOC、CAT活性、CO含量、GSH含量、GSH-px含量及SOD活性分别由(2.07±0.37) U/mg、(169.25±36.86) U/g、(1.35±0.32) μmol/g、(103.51±16.62) μmol/g、(38.40±7.97) μmol/g及(38.50±8.30) U/mg降低至(1.42±0.39) U/mg、(98.44±26.56) U/g、(0.96±0.21) μmol/g、(68.05±7.35) μmol/g、(23.83±5.04) μmol/g及(23.11±4.63) U/mg(P均<0.01)。二氧化硫供体干预后分别升高至(1.83±0.37) U/mg、(146.14±31.63) U/g、(1.28±0.20) μmol/g、(92.10±11.84) μmol/g、(37.16±3.01) μmol/g及(37.29±2.62) U/mg(P均<0.05)。
结论: 内源性二氧化硫在脓毒症发病过程中通过改善氧化应激平衡对心肌细胞起到保护作用。
Keywords: Endogenous sulfur dioxide; Myocardic injury; Oxidant stress; Sepsis.