A Comparative Study of Rutin and Rutin Glycoside: Antioxidant Activity, Anti-Inflammatory Effect, Effect on Platelet Aggregation and Blood Coagulation

The effects of rutin and rutin glycoside with different solubility were compared on antioxidant activity and anti-inflammatory effects in vitro and the effects on platelet aggregation and blood coagulation in vitro and in vivo. Rutin glycoside (consisting of rutin mono-glucoside and rutin di-glucoside) was prepared via enzymatic transglycosylation from rutin. Rutin glycoside showed a higher effect than rutin on radical scavenging activity in antioxidant assays. Rutin showed a higher toxicity than rutin glycoside in murine macrophage RAW264.7 cells. They had similar effects on the levels of nitric oxide (NO), prostaglandin E (PGE) 2 and pro-inflammatory cytokines (such as tumor necrosis factor (TNF)-α, and interleukin (IL)-6) in the cells. Both rutin and rutin glycosides similarly reduced the rate of platelet aggregation compared to controls in vitro. They also similarly delayed prothrombin time (PT) and activated partial thromboplastin time (APTT) in an in vitro blood coagulation test. The effect of repeated administration of rutin and rutin glycoside was evaluated in vivo using SD rats. The platelet aggregation rate of rutin and the rutin glycoside administered group was significantly decreased compared to that of the control group. On the other hand, PT and APTT of rutin and rutin glycoside group were not significantly delayed in vivo blood coagulation test. In conclusion, rutin and rutin glycoside showed differences in antioxidant activities in vitro, while they were similar in the reduction of NO, PGE2, TNF-α and IL-6 in vitro. Rutin and rutin glycoside also showed similar platelet aggregation rates, and blood coagulation both in vitro and in vivo condition. Comparing in vitro and in vivo, rutin and rutin glycoside were effective on platelet aggregation both in vitro and in vivo, but only in vitro on blood coagulation.

Prevention of Fatal Pulmonary Thromboembolism by Heparin Prophylaxis after Surgery for Hip Fractures

From 1960 through 1975, 337 patients with surgically treated acute fracture of the hip received subcutaneously administered aqueous heparin sodium to prevent thromboembolic episodes. Four hundred and three patients received no heparin. Their incidence of fatal pulmonary embolism was 3.5 percent. Ninety-five patients receiving the original “small dose” heparin regimen from August 1960 to November 1967 had a 4.2 percent incidence of fatal thromboembolism. These had been administered heparin 8-10 hours or less before surgery. Beginning November 1967 the “small dose” heparin schedule was altered in hip fracture patients to start heparin prophylaxis immediately following hospital admission. One hundred and forty-seven patients treated with the latter schedule had 0.0 percent fatal thromboembolism with the dose modified according to a coagulation time test. The patients received 2,500 units on admission and every 6 hours until the day before operation. Then they were given 5,000 to 10,000 units. 8 to 10 hours before surgery and 2,500 units every 6 hours after surgery until they were fully mobilized. The altered “small dose” heparin regimen adequately monitored by the blood coagulation test, the Dale and Laidlaw Coagulometer, proved highly effective as measured by fatality rates.