It has certain anti-inflammatory, liver cell membrane protection and liver function improvement effects. It can reduce the increase of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) caused by carbon tetrachloride, thioacetamide and D-aminogalactic acid, reduce the damage of D-aminogalactic acid to the liver and improve the chronic damage of immune factors to the liver.

This product is a non-steroidal anti-inflammatory drug, which inhibits cyclooxygenase and reduces prostaglandin synthesis to achieve anti-inflammatory and analgesic effects. Acute toxicity test results: the oral LD50 of rats is 534 mg/Kg, and the intraperitoneal injection LD50 is 575 mg/Kg; the oral LD50 of mice is 1234 mg/Kg, and the intraperitoneal injection LD50 is 435 mg/Kg.

This product is a non-steroidal anti-inflammatory drug that inhibits cyclooxygenase and reduces prostaglandin synthesis to achieve anti-inflammatory and analgesic effects.

This product is an amide local anesthetic. After blood absorption or intravenous administration, it has obvious biphasic effects of excitation and inhibition on the central nervous system, and there may be no precursor excitation. When the blood concentration is low, analgesia and drowsiness occur, and the pain threshold increases; with increasing doses, the effect or toxicity increases, and it has an anticonvulsant effect at sub-toxic blood concentrations; convulsions may occur when the blood concentration exceeds 5μg·ml-1. At low doses, this product can promote the outflow of K in myocardial cells, reduce myocardial autonomy, and have an anti-ventricular arrhythmia effect; at therapeutic doses, it has no obvious effect on the electrical activity of myocardial cells, atrioventricular conduction, and myocardial contraction; further increases in blood concentrations can cause a slowing of heart conduction velocity, atrioventricular conduction block, inhibition of myocardial contractility, and a decrease in cardiac output.