Protective effect of silymarin on rat liver injury induced by ischemia

Summary

The effect of silymarin on liver cell damage induced by ischemia was studied in rats fasted for 24 h. In the first series of experiments in vitro ischemia was induced by storing tissue blocks in closed vials at 37°C for 15, 30, 45 and 60 min. Cell injury was detected by the cytophotometrical measurement of glycogen phosphorylase activity in unfixed cryostat sections demonstrated by a modified histochemical procedure. In the second series of experiments in vivo ischemia was provoked by clamping the afferent vessels to the median and left lateral lobes of the liver for 60 min, followed by removal of the clamp and reperfusion. The extent of cell damage was determined by measuring the ALAT and ASAT activities in serum at 1, 3, 6 and 24 h after ischemia and by quantifying the extent of necrosis in the liver after 24 h reperfusion by measuring the unstained areas in cryostat sections incubated for lactate dehydrogenase activity. Silymarin (100mg/kg b.w.) was administered intravenously at 5 min before both the induction of ischemia and the restoration of blood flow (in vivo ischemia). Control received an equal amount of saline. The serum amino-transferase activities after 24 h reperfusion were significantly reduced in the silymarin-treated group (n=10); ALAT 293±193 U/L, ASAT 343±229 U/L compared with the control group (n=7): ALAT 1238±743 U/L, ASAT 948±541 U/L (p<0.03), and the extent of necrosis decreased from 25.6±16.0% (n=7) to 7.8±8.3% (n=10) (p<0.01) after treatment with silymarin. In addition, silymarin appeared to delay and diminish the marked decrease in glycogen phosphorylase activity during 60 min of in vitro ischemia. These results suggest that pretreatment intravenous silymarin can ameliorate hepatic injury associated with ischemia.