[Effect of electroacupuncture preconditioning on nitric oxide, nitric oxide synthase and oxyradical during hepatic ischemia-reperfusion injury in rabbits].
Jun Zhou, Ye Chen
Abstract
Jun Zhou, Ye Chen
Abstract
OBJECTIVE: To explore the effect of electroacupuncture preconditioning on hepatic ischemia-reperfusion injury and its mechanism. METHODS: Twenty-four rabbits were randomly divided into a sham operation (S) group, an ischemia-reperfusion (IR) group and an electroacupuncture preconditioning plus ischemia-reperfusion (EAP + IR) group, 8 cases in each group. Models of hepatic ischemia-reperfusion injury were produced in the groups EAP + IR and IR, and the rabbits in the group EAP + IR were treated with preoperative electroacupuncture at "Yang lingquan" (GB 34) for 30 min. The rabbits were sacrificed before ischemia or at 8 h, 24 h after ischemia-reperfusion, and the right hepatic lobes were collected to detect the content of nitric oxide (NO) and the induced nitric oxide synthase (iNOS). Moreover, blood samples (2 mL) were drawn from ear marginal artery to detect malondialdehyde (MDA) and superoxide dismutase (SOD). RESULTS: At 8 h and 24 h after hepatic ischemia-reperfusion, the content of NO [(0.491 +/- 0.102) micromol/g, (0.891 +/- 0.102) micromol/g], MDA [(5.94 +/- 0.35) micromol/L, (6.81 +/- 0.25) micromol/L)] and the activity of iNOS [(0.361 +/- 0.251) U/mg, (1.173 +/- 0.331) U/mg] in the group EAP + IR were significantly lower than those in the group IR [(0.756 +/- 0.087) micromol/g, (1.171 +/- 0.098) micromol/g, (6.36 +/- 0.21) micromol/L, (9.65 +/- 0.34) micromol/L, (0.692 +/- 0.223) U/mg, (1.711 +/- 0.323) U/mg, P < 0.05, P < 0.01], but the activity of SOD was significantly increased (P < 0.01). Compared with group S, the content of NO, MDA and the activity of iNOS in the groups EAP + IR and IR were significantly increased, but the activity of SOD were significantly decreased (all P < 0.01). CONCLUSION: Electroacupuncture preconditioning can inhibit the production of iNOS in liver, reduce the content of NO and MDA, and increase the activity of SOD so as to protect the liver.
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OBJECTIVE: To explore the effect of electroacupuncture preconditioning on hepatic ischemia-reperfusion injury and its mechanism. METHODS: Twenty-four rabbits were randomly divided into a sham operation (S) group, an ischemia-reperfusion (IR) group and an electroacupuncture preconditioning plus ischemia-reperfusion (EAP + IR) group, 8 cases in each group. Models of hepatic ischemia-reperfusion injury were produced in the groups EAP + IR and IR, and the rabbits in the group EAP + IR were treated with preoperative electroacupuncture at "Yang lingquan" (GB 34) for 30 min. The rabbits were sacrificed before ischemia or at 8 h, 24 h after ischemia-reperfusion, and the right hepatic lobes were collected to detect the content of nitric oxide (NO) and the induced nitric oxide synthase (iNOS). Moreover, blood samples (2 mL) were drawn from ear marginal artery to detect malondialdehyde (MDA) and superoxide dismutase (SOD). RESULTS: At 8 h and 24 h after hepatic ischemia-reperfusion, the content of NO [(0.491 +/- 0.102) micromol/g, (0.891 +/- 0.102) micromol/g], MDA [(5.94 +/- 0.35) micromol/L, (6.81 +/- 0.25) micromol/L)] and the activity of iNOS [(0.361 +/- 0.251) U/mg, (1.173 +/- 0.331) U/mg] in the group EAP + IR were significantly lower than those in the group IR [(0.756 +/- 0.087) micromol/g, (1.171 +/- 0.098) micromol/g, (6.36 +/- 0.21) micromol/L, (9.65 +/- 0.34) micromol/L, (0.692 +/- 0.223) U/mg, (1.711 +/- 0.323) U/mg, P < 0.05, P < 0.01], but the activity of SOD was significantly increased (P < 0.01). Compared with group S, the content of NO, MDA and the activity of iNOS in the groups EAP + IR and IR were significantly increased, but the activity of SOD were significantly decreased (all P < 0.01). CONCLUSION: Electroacupuncture preconditioning can inhibit the production of iNOS in liver, reduce the content of NO and MDA, and increase the activity of SOD so as to protect the liver.
Key concepts: Electroacupuncture, Malondialdehyde, Nitric oxide, Reperfusion injury, Ischemia, Medicine, Nitric oxide synthase, Superoxide dismutase