GABA content and an antioxidant profile positively correlated with the anticonvulsive activity of Microcos paniculata in acute seizure mice.

This study evaluated the effects of different parts of M. paniculata (MP) extracts on convulsions and antioxidant activities in mice. Six polyphenolic compounds were identified, where epicatechin and quercetin have been identified in the highest amounts (23.01 and 32.23 mg/100 g of dry MP extract, respectively) in MP leaf and stem extracts, using Ultra Performance Liquid Chromatography. 7-day oral administration of MP at doses of 100, 200, and 400 mg/kg body weight (BW) significantly reduced convulsions and reduced mortality rates compared with seizure inducer groups. Antioxidant potentials were measured by superoxide dismutase (SOD), catalase (CAT), thiobarbituric acid reactive substances (TBARS), and reduced glutathione (GSH) content in whole-brain homogenates. Gamma-aminobutyric acid (GABA) levels significantly increased in leaves and stem-treated groups, suggesting that MP leaves and stems have potent antioxidant properties that can attenuate convulsions by modulating the GABAergic system and antioxidant activities.

Antiplatelet activity of Phellinus baummii methanol extract is mediated by cyclic AMP elevation and inhibition of collagen-activated integrin-α(IIb) ß3 and MAP kinase.

Phellinus baumii is a mushroom that has been used as folk medicine against various diseases and is reported to have antidiabetic, anticancer, antioxidant, antiinflammatory and antihypertensive activities. However, information on the effects of P. baumii extract in platelet function is limited. Therefore, the aim of this study was to examine the impact of a P. baumii methanol extract (PBME) on platelet activation and to investigate the mechanism behind its antiplatelet activity. PBME effects on agonist-induced platelet aggregation, granule secretion, [Ca²âº](i) mobilization, α(IIb) ß3 activation, cyclic AMP release and mitogen-activated protein kinase (MAPK) phosphorylations were studied using rat platelets. PBME dose-dependently inhibited collagen, thrombin and ADP-induced platelet aggregation with an IC50 of 51.0 ± 2.4, 54.0 ± 2.1 and 53.0 ± 4.3 µg/mL, respectively. Likewise, thrombin-induced [Ca²âº](i) and collagen-activated ATP secretions were suppressed in PBME treated platelets. Aggregation and ATP secretion were also markedly attenuated by PBME alone or in combination with PP2 (Src inhibitor) and U-73122 (PLC inhibitor) in collagen-stimulated platelets. Besides, PBME treatment elevated basal cyclic AMP levels and inhibited collagen-induced integrin-α(IIb) ß3 activation. Moreover, PBME attenuated extracellular-signal-regulated protein kinase 2 (ERK2) and c-Jun N-terminal kinase 1 (JNK1) phosphorylations. Further PD98059 (ERK inhibitor) and SP60025 (JNK inhibitor) reduced collagen-induced platelet aggregation and ATP secretion. In conclusion, the observed PBME antiplatelet activity may be mediated by activation of cyclic AMP and inhibition of ERK2 and JNK1 phosphorylations. Finally, these data suggest that PBME may have therapeutic potential for the treatment of cardiovascular diseases that involve aberrant platelet function.

Inhibitory effects of Bulnesia sarmienti aqueous extract on agonist-induced platelet activation and thrombus formation involves mitogen-activated protein kinases.

ETHNOPHARMACOLOGICAL RELEVANCE: B. sarmienti has long been recognized in folk medicine as a medicinal plant with various medicinal uses. Traditionally, it has been appreciated for the skin-healing properties of its essence. The bark has also been employed to treat stomach and cardiovascular disorders and reported to have antitumor, antioxidant and anti-inflammatory activities. However, information on its antiplatelet activity is limited. AIM OF THE STUDY: To examined the effects of B. sarmienti aqueous extract (BSAE) in platelet physiology. MATERIALS AND METHODS: The anti-platelet activity of BSAE was studied using rat platelets for in vitro determination of the extract effect on agonist-induced platelet aggregation, ATP secretion, [Ca(2+)](i) mobilization and MAP kinase phosphorylation. The extract in vivo effects was also examined in arterio-venous shunt thrombus formation in rats, and tail bleeding time in mice. RESULT: HPLC chromatographic analysis revealed that B. sarmienti extract contained (+)-catechin (C), (-)-epigallocatechin (EGC), (-)-epicatechin (EC), and (-)-epicatechin gallate (ECG). BSAE, significantly and dose dependently, inhibited collagen, thrombin, or ADP-induced platelet aggregation. The 50 percent inhibitory concentrations (IC(50)) of the extract for collagen, thrombin and ADP-induced platelet aggregation were 45.3+/-2.6, 100+/-5.6 and 110+/-4.6 microg/ml, respectively. Collagen activated ATP release and thrombin-induced intracellular Ca(2+) concentration were reduced in BSAE-treated platelets. In addition, the extract in vivo activity showed that BSAE at 100 mg/kg significantly attenuated thrombus formation in rat extracorporeal shunt model while mice tail bleeding time was not affected. Moreover, BSAE attenuated p38 mitogen-activated protein kinase (p38 MAPK), c-Jun N-terminal kinase 1 (JNK1) and extracellular-signal-regulated protein kinase 2 (ERK2) phosphorylations. CONCLUSION: BSAE inhibits platelet activation, granule secretion, aggregation, and thrombus formation without affecting bleeding time, and that this effect is mediated by inhibition of P38, JNK1 and ERK2 phosphorylations. The ability of BSAE to inhibit platelet function might be relevant in cases involving aberrant platelet activation where the plant extract could be considered as a candidate to anti-platelet and antithrombotic agent.