| Aim: Amanita mushroom poisoning, which can induce damages ofsome important organs including heart, liver and kidney, is oftenhappening in clinic emergency treatment. The aim of the present studywas to explore (1) the damages of amanita and its major toxic substanceα-amanitin on hepatic and cardiac tissues and function and (2) theprotective effects of Ganoderma lucidum (GL) on amanita-inducedhepatic and cardiac damages.Methods: (1) In vivo experiment: New Zealand rabbits were dividedat random into four groups: control group; amanita-treated group, orallytreatment with amanita (0.1 g/kg); two different doses of GL-treatedgroups, 20 g/kg or 60 g/kg GL decoction was orally treated for 5consecutive days after treatment with amanita. At the end of theexperiments, the blood samples of all animals were collected to determineactivities of serum maker enzymes reflecting hepatic function (ALT,T-BIL, TP and ALB) and cardiac function (AST, LDH,α-HBDH, CK,CK-MB), and the tissue samples of both liver and heart were collected toobserve histological changes. (2) In vitro experiment: SD rats were orallytreated with different concentrations of GL decoction (10, 20 or 40 g/kg)containing 8 g/ml rude GL herb for serve consecutive days and then theserum with different concentrations of GL was prepared. Similarly, serumwithout GL was prepared through treatment SD rats with distilled water(10 ml/kg). In cultured human hepatic cell line HL-7702 and myocardialcell line H9c2,α-amanitin (5μg/ml or 20μg/ml) was treated in presence or absence of serum with different GL for 24 or 48 hours. At the end ofthe experiment, the cell viability and apoptosis were determined by MTTtest and flow cytometry, respectively, and the cultured medium wascollected to determine the maker enzymes activities reflecting liverfunction (including ALT and AST) and cardiac function (including AST,LDH,α-HBDH).Results: (1) The livability of animals in amanita-treated group was60％, and the livability of others was 100％. At second day, serumactivities of both ALT and T-BIL in amanita-treated group were markedlyhigher than those in control group, in the contrary, serum level of both TPand ALB were significantly lower in amanita-treated group compared tocontrol group. All enzyme activities reflecting cardiac function weremarkedly increased in amanita-treated group. Orally treatment with GLdecoction (20 g/kg or 60 g/kg) for 5 d markedly attenuated the changes inthese parameters reflecting hepatic and cardiac function mentioned aboveinduced by amanita. (2) In cultured hepatic cells, treatment withα-amanitin for 24 h markedly decreased cell viability and increased ALTand AST activities in the cultured medium. Serum with GL markedlyattenuated these adverse effects ofα-amanitin on hepatic cells. (3) Asshown by results of flow cytometry, treatment withα-amanitin couldsignificantly induced apoptotic death of hepatic cells. Both serum withGL and normal serum markedly inhibitedα-amanitin-induced apoptosisof hepatic cells. Moreover, there is no significant different of cellapoptosis ratio between serum with GL and normal serum groups. (4) Incultured cardiac cells, treatment withα-amanitin for 48 h could markedlydecrease cell viability and increase the activities of AST, LDH andα-HBDH in cultured medium. Serum with GL markedly attenuated thesetoxic effects ofα-amanitin on cardiac cells. Conclusions: (1) Amanita and its major substanceα-amanitin havestrong toxicity to liver and heart, and their effects might be related todamaging hepatic and cardiac functions and inducing cell apoptosis. (2)GL markedly improved the livability of amanita-treated animals andattenuated amanita-induced damages of hepatic and cardiac cells.
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