An experimental study on the mechanism of anisodamini hydrobromidum in treating acute ischemic renal failure.
In order to explore the mechanism of anisodamini hydrobromidum (654-2) in treating acute ischemic renal failure, the model of acute ischemic renal failure in white New Zealand rabbits was established to dynamically observe and statistically analyze the intracellular concentration changes of free calcium ([Ca2+]i) and inositol triphosphate (IP3). The results showed that the levels of [Ca2+]i and IP3 in acute renal failure group were higher than those in control group (P < 0.01). However, the levels of [Ca2+]i and IP3 in 654-2 treated group were significantly lower than those in acute renal failure group (P < 0.001). It was concluded that 654-2 could alleviate Ca(2+)-overload in renal histocytes in acute ischemic renal failure. The protective mechanism is associated with intracellular reduction of IP3.
Liu
X
X
Department of Internal Medicine, Tongji Hospital, Tongji Medical University, Wuhan.
Zhang
J
J
D058186:Acute Kidney Injury / Q000188:drug therapy / Q000378:metabolism*; D000818:Animals; D001693:Biological Transport, Active; D002118:Calcium / Q000378:metabolism*; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D005260:Female; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism; D008297:Male; D011817:Rabbits; D011897:Random Allocation; D012991:Solanaceous Alkaloids / Q000494:pharmacology*
D004365:Drugs, Chinese Herbal; D012991:Solanaceous Alkaloids; C003922:anisodamine; D015544:Inositol 1,4,5-Trisphosphate; D002118:Calcium