Effect of ginseng and prepared aconite injection on TXA2/PGI2 and nuclear factor-κB in rat model of hepatic ischemia-reperfusion

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AIM: To explore the protective effects of ginseng and prepared aconite (Shen Fu) injection on the TXA2/PGI2 and nucleus factorκB (NF-κB) in a rat model of hepatic ischemia-reperfusion (IR). METHODS: Twenty-four male Wistar rats weighing 200-250g were randomly divided into Shen Fu (SF) group treated with intraperitoneal SF injection (10 mL/kg) and IR group treated with 0.9% sodium chloride solution (10 mL/kg) as control group. Hepatic ischemia was induced by Pringle s maneuver for 15 minutes, and then reperfusion was performed for one or three hours. Venous blood samples were collected three hours after reperfusion for measurement of TXB2 and 6-keto-PGF(subscript 1α). Liver tissue samples were collected one or three hours after reperfusion, for measurement of deoxidized glutathione (GSH) and morphological and immunochemical studies. RESULTS: Plasma TXB2 was lower in the SF group than in the JR group after three-hour reperfusion (118.7±19.1 vs 386.3±282.7, P＞0.05), while 6-keto-PGF(subscript 1α) was higher in the SF group than in the IR group (1081.7±282.7 vs 960.0±209.9, P＞0.05). The ratio of TXB2 and 6-keto-PGF(subscript 1α) (0.11±0.03 vs 0.39±0.24, P＜0.05) was significantly lower in the SF group. Fifteen minutes after ischemia and one hour after reperfusion, NF-κB p65 was expressed in hepatocytes and Kuffer cells. The percentage of NF-κB p65 positive cells in the SF group was significantly lower (59.33%±11.06% vs 75.83%±11.46%, P＜0.05) and GSH was slightly higher (47.59±19.07 vs 37.32±4.71, P＞0.05) than those in the IR group. Three-hour reperfusion fifteen minutes after ischemia caused important histologic alterations in the liver. Marked structural abnormalities were observed in the IR group, such as massive hepatocyte swelling, necrosis, mitochondria edema and vacuolar changes. In the SF group, hepatic tissue injury was significantly improved. CONCLUSION: Shen Fu injection protects hepatic tissue from ischemia-reperfusion injury by decreasing the ratio of thromboxane A2 and prostacyclin and inhibiting the activation of NF-κB.