中华航海医学与高气压医学杂志
中華航海醫學與高氣壓醫學雜誌
중화항해의학여고기압의학잡지
CHINESE JOURNAL OF NAUTICAL MEDICINE AND HYPERBARIC MEDICINE
2011年
4期
214-216
,共3页
李厚成%罗杰%刘培%李彬彬%刘玉%吴建平%宁红平
李厚成%囉傑%劉培%李彬彬%劉玉%吳建平%寧紅平
리후성%라걸%류배%리빈빈%류옥%오건평%저홍평
脓毒症%细胞凋亡%高压氧
膿毒癥%細胞凋亡%高壓氧
농독증%세포조망%고압양
Sepsis%Apoptosis%Hyperbaric oxygen
目的 观察高压氧对大鼠脓毒症膈肌p38促分裂素原活化蛋白激酶(mitogen-activated protein kinases,MAPK)信号通路的影响,以探讨其对脓毒症膈肌损伤的保护作用。方法 SPF级成年雄性SD大鼠30只,采用数字表法随机分为A组(假手术组,n=10)、B组(脓毒症组,n=10)及C组(高压氧治疗组,n=10)。其中A组在给予水合氯醛麻醉成功后,从正中线剪开大鼠腹部,然后缝合伤口。B组和C组在麻醉成功后,使用盲肠结扎穿刺(cecal ligation and puncture,CLP)模型将大鼠制成脓毒症动物模型,并且C组在术后立即行高压氧治疗。所有大鼠在术后16 h处死,取左侧膈肌检测肌条收缩力,右侧膈肌检测膈肌肌细胞凋亡率及p38 MAPK蛋白表达。结果 B组与A组比较,膈肌肌细胞凋亡率及p38 MAPK蛋白表达明显上升,肌条收缩力明显下降,2组比较差异有统计学意义(P<0.01)。给予高压氧治疗后,膈肌细胞凋亡率、p38 MAPK蛋白表达及肌条收缩力较脓毒症组明显恢复,2组比较差异有统计学意义(P<0.01)。结论 高压氧能够有效抑制脓毒症时p38 MAPK蛋白的表达,减少膈肌肌细胞凋亡率,从而减轻脓毒症膈肌损伤。
目的 觀察高壓氧對大鼠膿毒癥膈肌p38促分裂素原活化蛋白激酶(mitogen-activated protein kinases,MAPK)信號通路的影響,以探討其對膿毒癥膈肌損傷的保護作用。方法 SPF級成年雄性SD大鼠30隻,採用數字錶法隨機分為A組(假手術組,n=10)、B組(膿毒癥組,n=10)及C組(高壓氧治療組,n=10)。其中A組在給予水閤氯醛痳醉成功後,從正中線剪開大鼠腹部,然後縫閤傷口。B組和C組在痳醉成功後,使用盲腸結扎穿刺(cecal ligation and puncture,CLP)模型將大鼠製成膿毒癥動物模型,併且C組在術後立即行高壓氧治療。所有大鼠在術後16 h處死,取左側膈肌檢測肌條收縮力,右側膈肌檢測膈肌肌細胞凋亡率及p38 MAPK蛋白錶達。結果 B組與A組比較,膈肌肌細胞凋亡率及p38 MAPK蛋白錶達明顯上升,肌條收縮力明顯下降,2組比較差異有統計學意義(P<0.01)。給予高壓氧治療後,膈肌細胞凋亡率、p38 MAPK蛋白錶達及肌條收縮力較膿毒癥組明顯恢複,2組比較差異有統計學意義(P<0.01)。結論 高壓氧能夠有效抑製膿毒癥時p38 MAPK蛋白的錶達,減少膈肌肌細胞凋亡率,從而減輕膿毒癥膈肌損傷。
목적 관찰고압양대대서농독증격기p38촉분렬소원활화단백격매(mitogen-activated protein kinases,MAPK)신호통로적영향,이탐토기대농독증격기손상적보호작용。방법 SPF급성년웅성SD대서30지,채용수자표법수궤분위A조(가수술조,n=10)、B조(농독증조,n=10)급C조(고압양치료조,n=10)。기중A조재급여수합록철마취성공후,종정중선전개대서복부,연후봉합상구。B조화C조재마취성공후,사용맹장결찰천자(cecal ligation and puncture,CLP)모형장대서제성농독증동물모형,병차C조재술후립즉행고압양치료。소유대서재술후16 h처사,취좌측격기검측기조수축력,우측격기검측격기기세포조망솔급p38 MAPK단백표체。결과 B조여A조비교,격기기세포조망솔급p38 MAPK단백표체명현상승,기조수축력명현하강,2조비교차이유통계학의의(P<0.01)。급여고압양치료후,격기세포조망솔、p38 MAPK단백표체급기조수축력교농독증조명현회복,2조비교차이유통계학의의(P<0.01)。결론 고압양능구유효억제농독증시p38 MAPK단백적표체,감소격기기세포조망솔,종이감경농독증격기손상。
Objective To explore the effect of hyperbaric oxygen(HBO) on the signal pathway of p38 mitogen-activated protein kinases (MAPK) in rats with diaphragmatic damage induced by sepsis, and also to investigate the protective effect of HBO on diaphragmatic damage. Methods Thirty adult SD rats were randomly divided into 3 groups: Group A (the sham operation group, n = 10), Group B (the sepsis group, n= 10) and Group C ( the HBO group, n = 10). Following anesthesia with choral hydrate, the rats of Group A were cut in the mid line of the abdomen, and were then sutured. Sepsis model was established by using cecal ligation and puncture (CLP) for the animals in group B and C, and the rats in Group C were immediately treated with HBO following surgery. All the rats were sacrificed 16 hours after surgery. Diaphragm muscles on the left side were taken to measure the contracti1e force and diaphragm muscles on the right side were taken to detect the apoptosis rate and the expression of p38 MAPK. Results The apoptosis rate of diaphragm muscles and positive expression rate of p38 MAPK for the rats in Group B increased significantly, when they were compared with those of the rats in Group A. The contractile force of diaphragm muscles decreased with statistical significance, when a comparison was made between the 2 groups (P < 0.01 ). Following HBO therapy, the apoptosis rate of diaphragmatic muscles, the expression rate of p38 MAPK and the contractile force of the animals in group B improved obviously and statistical significance could be doted between the 2 groups (P <0. 0 1 )Conclusions H BO could effectively inhibit the expression rate of p38 M APK, decrease the apoptosis rate of diaphragm muscles, thus alleviating lesion of diaphragmatic muscles induced by sepsis.