Extract ofAntrodia camphorataExerts Neuroprotection against Embolic Stroke in Rats without Causing the Risk of Hemorrhagic Incidence

Abstract

In this study, the neuroprotective effect of an extract of Antrodia camphorata (A. camphorata), a fungus commonly used in Chinese folk medicine for treatment of viral hepatitis and cancer, alone or in combination with aspirin was investigated in a rat embolic stroke model. An ischemic stroke was induced in rats by a selective occlusion of the middle cerebral artery (MCA) with whole blood clots and then orally treated with A. camphorata (0.25 and 0.75 g/kg/day) alone and combined with aspirin (5 mg/kg/day). Sixty days later, the brains were removed, sectioned, and stained with triphenyltetrazolium chloride and analysed by a commercial image processing software program. Brain infarct volume, neurobehavioral score, cerebral blood perfusion, and subarachnoid and intracerebral hemorrhage incidence were perceived. In addition, potential bleeding side effect of the combinative therapy was assessed by measuring hemoglobin (Hb) content during intracerebral hemorrhage and gastric bleeding, prothrombin time (PT), and occlusion time (OT) after oral administration. Posttreatment with high dose A. camphorata significantly reduced infarct volume and improved neurobehavioral score (P < 0.05). Since A. camphorata alone or with aspirin did not alter the Hb level, this treatment is safe and does not cause hemorrhagic incident. Remarkably, the combination of A. camphorata and aspirin did not show a significant effect on the bleeding time, PT and OT increase suggesting that A. camphorata may have the neuroprotective effect without the prolongation of bleeding time or coagulation time. From these observations, we suggest that combinative therapy of A. camphorata and aspirin might offer enhanced neuroprotective efficacies without increasing side effects.

Protective Effect of Antrodia Camphorate on the Tissues of Brain, Kidney, Lung, and Liver Is Correlated with Declining Lipid Peroxidation

“…In this regard, higher MDA level represents elevated oxidative stress and injury has been well-recognized. Our present observation indicated that Antrodia Camphorata can significantly inhibit free radicalmediated lipid peroxidation, and our present finding was in according with the previous investigation [9][10][11][12][13]18].…”

“…Furthermore, in vivo study has indicated that Antrodia Camphorata not only can elevate hepatic glutathione-dependent enzymes upon protecting chemical-induced lesion on rat liver but also may decline oxidative injury conducted by toxic molecules of hydrogen peroxide [7]. On the other hand, previous experiment has indicated that cerebral ischemia-induced brain infarction and neurobehavioral disorder can be improved via administration of the traditional Chinese Medicine of Antrodia Camphorata [8][9][10][11][12]. As mentioned above, it seems likely to emphasize its beneficial effect here that Antrodia Camphorate may exactly exert its excellent antioxidant ability to alleviate further oxidative lesion.…”

The neuroprotective effects of Tao-Ren-Cheng-Qi Tang against embolic stroke in rats

“…All of the rats were kept at 37 °C in groups of five under a 12-h dark/light cycle with ad libitum access to food and water before the surgery. The rats were subjected to MCAO-induced ischemia by the administration of an autologous blood clot, as described in our previous studies [ 11 , 12 ]. After surgery, the rats were housed individually under similar environmental conditions and were found to be free of apparent infection or inflammation, as well as showing no neurological deficits.…”

Current and further outlook on the protective potential of Antrodia camphorata against neurological disorders

“…It has been reported that AC could effectively prevent serum-deprived apoptosis of PC12 cells by increasing phosphorylated ERK and decreasing phosphorylated JNK and p38, and by regulating a PKA/CREB-dependent pathway ( Huang et al, 2005 ; Lu et al, 2008 ). Oral treatment of AC extract provided neuroprotection in rats with thromboembolic stroke by reducing infarct volume, improves neurological outcome ( Lee et al, 2014 ). Furthermore, downregulation of iNOS/HO-1/Bax/caspase-3 and inhibition of hydroxyl radical formation were the main molecular pathways behind the AC neuroprotective activity against cerebral ischemia in rats ( Yang et al, 2015 ).…”