Cyclophosphamide protects against myocardial ischemia/reperfusion injury in rats: one of the therapeutic targets is high sensitivity C-reactive protein.

OBJECTIVE: Cyclophosphamide has a role of decreasing high-sensitivity C-reactive protein in the treatment of autoimmune disorders. The effect of cyclophosphasmide on high-sensitivity C-reactive protein was investigated in myocardial ischemia/reperfusion rat. METHODS: Open-chest rats were submitted to 30 minutes of ischemia and followed for 3, 12, or 24 hours of reperfusion. All 72 rats survived and were divided into sham, ischemia/reperfusion (I/R) and cyclophosphamide groups, and each group included 3 time-point subgroups (3, 12, and 24 hours; n = 8 for each subgroup). Cyclophosphamide (0.75 g/m(2)) or saline was intraperitoneally administrated in the cyclophosphamide or I/R group. A polyethylene tube was inserted into the left ventricular cavity to detect left ventricular systolic pressure, left ventricular end-diastolic pressure, and maximum rate of rise or fall of left ventricular pressure. In the end, blood was collected for detection of high-sensitivity C-reactive protein, and hearts were harvested for histopathologic assessment and infarct size determination. RESULTS: Compared with the I/R group, rats treated with cyclophosphamide showed a significant recovery in myocardial function with improved left ventricular systolic pressure (88.27 +/- 3.78 vs 68.62 +/- 3.78 mm Hg at 3 hours, 92.04 +/- 3.77 vs 63.74 +/- 4.87 mm Hg at 12 hours, and 90.41 +/- 3.98 vs 64.21 +/- 4.88 mm Hg at 24 hours; P < .05, respectively). Left ventricular end-diastolic pressure and maximum rate of rise or fall of left ventricular pressure also had similar trends. Infarct size was reduced (26.1% +/- 0.4% vs 40.4% +/- 0.4% at 3 hours, 21.6% +/- 0.4% vs 49.9% +/- 0.4% at 12 hours, and 21.6% +/- 0.4% vs 40.0% +/- 0.4% at 24 hours; P < .01, respectively). Histopathologic damage score was attenuated (1.83 +/- 0.14 vs 2.17 +/- 0.14 at 3 hours, 2.33 +/- 0.14 vs 3.17 +/- 0.14 at 12 hours, and 2.83 +/- 0.14 vs 3.83 +/- 0.14 at 24 hours; P < .01, respectively). Plasma high-sensitivity C-reactive protein concentration was significantly reduced (29.28 +/- 0.51 vs 32.26 +/- 0.51 ng/mL at 3 hours, 29.06 +/- 0.50 vs 31.8 +/- 0.51 ng/mL at 12 hours, and 28.61 +/- 0.51 vs 31.86 +/- 0.51 ng/mL at 24 h; P < .01, respectively). CONCLUSION: Cyclophosphamide protects myocardial ischemia/reperfusion injury in the rat with a decrease in plasma concentration of high-sensitivity C-reactive protein.

[Effect of acupoint-injection of oxymatrine on experimental hepatic carcinoma and study on the mechanism].

OBJECTIVE: To investigate the effect of acupoint injection of oxymatrine (OM) on experimental hepatocellular carcinoma and the mechanism. METHODS: The rats of hepatocellular carcinoma induced by 2-acetoaminoflurence (2-AAF) were randomly divided into a normal control group (group N), a model group (group M), a control group of oxymatrine intraperitoneal injection (OM ip group) and a treatment group of small dose oxymatrine injection into Zusanli (OM ZSL group). At the end of 12h week, the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transferase (gamma-GT) were determined. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expressions of cyclin D1 and cyclin-dependent kinase 4 (CDK4) mRNA in hepatocellular carcinoma tissues. RESULTS: The number of cancer nodes on the surface of liver in th Om ip group and the Om ZSL group was lower than in the group M, with the serum ALT, AST, and gamma-GT levels significantly decreased (P<0. 01), and significantly inhibited expressions of cyclin D1, CDK4 mRNA (P<0. 01). CONCLUSION: OM ip and small dose oxymatrine injection into ZSL can treat or delay hepatocarcinogenisis of hepatocellular carcinoma induced by 2-AAF. Partial mechanism of this anti-carcinoma is protecting hepatocytes possibly through improving hepatic functions, and inhibiting excessive proliferation of liver cancer cells via inhibiting the expressions of cyclin Dl, CDK4 mRNA.