This product is a long-acting non-steroidal anti-inflammatory drug. It can inhibit the activity of cyclooxygenase and reduce the synthesis of prostaglandins. Animal experiments show that the anti-inflammatory and analgesic effects of this product are weaker than indomethacin, but stronger than aspirin.

1. Effects on water and electrolyte excretion. (1) Diuretic effect. Urinary excretion of sodium, potassium, chloride, phosphorus and magnesium ions increases, while urinary excretion of calcium decreases. The mechanism of action of this type of drug is mainly to inhibit the reabsorption of sodium chloride in the distal tubule anterior segment and the proximal tubule (less severe), thereby increasing the Na⁺-K⁺ exchange in the distal tubule and collecting duct, and increasing K⁺ secretion. Its mechanism of action is not yet fully understood. This type of drug can inhibit carbonic anhydrase activity to varying degrees, which can explain its effect on the proximal tubule. This type of drug can also inhibit phosphodiesterase activity, reduce the renal tubular uptake of fatty acids and mitochondrial oxygen consumption, thereby inhibiting the active reabsorption of Na⁺ and Cl⁻ by the renal tubule. (2) Antihypertensive effect. In addition to the diuretic and sodium excretion effects, there may be extrarenal mechanisms involved in antihypertensive effects, which may be to increase the excretion of Na⁺ in the gastrointestinal tract. 2. Effects on renal hemodynamics and glomerular filtration function. Due to the reduced reabsorption of water and Na⁺ by the renal tubules, the increased pressure in the renal tubules, and the increased water and Na⁺ flowing through the distal convoluted tubules, the macula densa is stimulated to increase the secretion of renin and angiotensin in the kidney through the tubular-glomerular reflex, causing renal vasoconstriction, decreased renal blood flow, constriction of the glomerular afferent and efferent arterioles, and a decrease in the glomerular filtration rate.

It can directly inhibit the Na⁺-K⁺ exchange in the distal tubules and collecting ducts of the kidney, thereby increasing the excretion of Na⁺, Cl⁻, and water, and reducing the excretion of K. When the two are used together, the diuretic effect is enhanced and the adverse reactions (hydrochlorothiazide causes hypokalemia while triamterene can retain potassium) are reduced.

It competes with p-aminobenzoic acid for dihydrofolate synthase, hindering bacterial synthesis of dihydrofolate; when used in combination with trimethoprim, it double blocks bacterial tetrahydrofolate synthesis, enhancing the antibacterial effect

It competes with p-aminobenzoic acid for dihydrofolate synthase, hindering bacterial synthesis of dihydrofolate; when used in combination with trimethoprim, it double blocks bacterial tetrahydrofolate synthesis, enhancing the antibacterial effect

Inhibits bacterial dihydrofolate reductase, hindering the reduction of dihydrofolate to tetrahydrofolate; when used in combination with sulfonamides, it double blocks the synthesis of bacterial tetrahydrofolate and enhances the antibacterial effect

Hyodeoxycholic acid has a significant expectorant effect, a significant antipyretic effect on experimental guinea pigs, an anticonvulsant effect, and a synergistic effect with barbiturates.

It can antagonize the contraction or contracture of the gastrointestinal tract, trachea, bronchi or bronchiolar smooth muscle caused by histamine, and relieve the spasm and congestion effects of histamine on bronchial smooth muscle. The antiemetic effect may be related to the inhibition of the emetic chemoreceptor area in the medulla oblongata. The mechanism of inhibition of the central nervous system is not yet clear, but it may be due to indirectly reducing the excitability of the brainstem reticular formation activation system.