OBJECTIVETo investigate the effects of Radix Salviae Miltiorrhiae, Radix Aconiti Lateralis Preparata and Rhizoma Anemarrhena on nitric oxide (NO) system of heart, liver, intestine, lung, kidney and serum in mice with endotoxemia, and to explore the potential molecular mechanism of the three kinds of traditional Chinese drugs.

METHODSModel mice of endotoxemia were established by intraperitoneally injected with E. coli. endotoxin at the dose of 6 mg/kg. The levels of NO, nitric oxide synthase ( NOS) and superoxide dismutase ( SOD) in heart, liver, intestine, lung, kidney and serum of mice were measured at the points after injection for 4 hours, 8 hours and 24 hours, respectively.

RESULTS(1) Radix Salviae Miltiorrhiae could significantly increase the contents of constitutive nitric oxide synthase (cNOS) and SOD in the above tissues and serum, while decrease the content of inducible nitric oxide synthase (iNOS). (2) As compared with the model group, Radix Aconiti Lateralis could significantly decrease the contents of iNOS and NO, increase content of SOD in heart, lung and kidney tissues. (3) N.-Nitro-L-arginine (L-NNA) significantly decreased the content of iNOS, NO and SOD in all above tissues and serum, and also decreased the content of cNOS in lung and kidney tissues and serum. (4) Rhizoma Anemarrhenae could significantly increase the concentrations of iNOS and NO and decrease content of SOD in liver, lung and kidney tissues than those in the model group.

CONCLUSIONRadix Salviae Miltiorrhiae and Radix Aconiti Lateralis have a protective effect on the endotoxemia mice by suppressing the content of iNOS to reduce the production of NO induced by iNOS. At the same time, Radix Salviae Miltiorrhiae can improve the mice symptoms by increasing the beneficial NO through the increasing production of cNOS. Rhizoma Anemarrhenae can aggravate the injury of endotoxemia mice by increasing the production of NO due to producing large numbers of iNOS. L-NNA, non-selective inhibitor of NOS, aggravates damage of tissues and increases mortality, though it can reduce the increase of iNOS and NO induced by lipopolysaccharide.