RESUMEN
Sanghuangporus toxicodendri (Hymenochaetales) is described as new based on collections made from Shennongjia Forestry District, Hubei Province, China. All studied basidiocarps grew on living trunks of Toxicodendron sp. This new species is characterized by having perennial, effused-reflexed to pileate basidiocarps; pore surface brownish yellow or yellowish brown, pores 7-9 per mm; context 1-5 mm thick or almost invisible; setae ventricose, dark brown, 26-42 × 7-10 µm; basidia 4-sterigmate or occasionally 2-sterigmate; basidiospores broadly ellipsoid, smooth, brownish yellow, slightly thick-walled, mostly 3.5-4 × 2.8-3 µm. Maximum likelihood and Bayesian inference phylogenies inferred from internal transcribed spacer (ITS) region of rDNA indicated that Sanghuangporus spp. formed a monophyletic clade and resolved as a sister to Tropicoporus spp., and six strains of S. toxicodendri formed a monophyletic group which is sister to S. quercicola. An identification key to known species of Sanghuangporus is provided.
RESUMEN
Aim. To study the effect and mechanism of traditional Chinese medicine Qinbai Qingfei concentrated pellet (QQCP) against Mycoplasma pneumoniae (MP). Methods. Rat airway smooth muscle (ASM) cells were used to examine the antimycoplasmal activity of QQCP via four drug-adding modes: pre- and postadding drugs, simultaneous-adding after drug and MP mixed, and simultaneous-adding drug and MP; taking roxithromycin dispersive tablets (RDT) as positive control, the cellular A 570 values were determined by MTT method. Results. All of A 570 values in QQCP group were significantly higher than those of the corresponding MP control group (P < 0.01) in four drug-adding modes; there was no significant difference in A 570 values between the QQCP group and that of the positive control group (P > 0.05), confirming that QQCP could significantly inhibit the infectivity of MP to ASM cells. Conclusion. QQCP had significant activity in preventing and treating MP infection, killing MP, and antiabsorption.
RESUMEN
The present study aimed to examine the protective effect of ginsenoside Rg1 against colistin-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. Ginsenoside Rg1 was shown to elevate cell viability, decrease levels of malondialdehyde and intracellular reactive oxygen species, enhance activity of superoxide dismutase and glutathione, and decrease the release of cytochrome-c, formation of DNA fragmentation in colistin-treated PC12 cells. Ginsenoside Rg1 also reversed the increased caspase-9 and -3 mRNA levels caused by colistin in PC12 cells. These results suggest that ginsenoside Rg1 exerts a neuroprotective effect on colistin-induced neurotoxicity in PC12 cells, at least in part, via the inhibition of oxidative stress, prevention of apoptosis mediated via mitochondria pathway. Co-administration of ginsenoside Rg1 highlights the potential to increase the therapeutic index of colistin.