• Mycobiology
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• 제47권4호
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• pp.408-414
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• 2019

Crinum asiaticum and Hymenocallis littoralis, commonly known as spider lilies are bulbous perennial and herbaceous plants that widely planted in Malaysia as ornamental. During 2015-2016, symptom of leaf blight was noticed on the hosts from several locations in Penang. The symptom appeared as irregular brown to reddish lesions surrounded by yellow halos. As the disease progressed, the infected leaves became blighted, dried, and fell off with the presence of black microsclerotia and pycnidia on the lesions parts. The present study was conducted to investigate the causal pathogen of leaf blight on C. asiaticum and H. littoralis. Based on morphological characteristics and DNA sequences of internal transcribed spacer (ITS) region and translation elongation factor 1-alpha (TEF1-α) gene, the causal pathogen was identified as Macrophomina phaseolina. Phylogenetic analysis of combined dataset of ITS and TEF1-α grouped the isolates studied with other isolates of M. phaseolina from GenBank. The grouping of the isolates was supported by 96% bootstrap value. Pathogenicity test proved the role of the fungus in causing leaf blight on both hosts.

• Asian Pacific Journal of Cancer Prevention
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• 제15권21호
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• pp.9319-9325
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• 2014

Alkaloids are the most extensively featured compounds of natural anti-tumor herbs, which have attracted much attention in pharmaceutical research. In our previous studies, a mixture of major three alkaloid components (5, 6-dihydrobicolorine, 7-deoxy-trans-dihydronarciclasine, littoraline) from Hymenocallis littoralis were extracted, analyzed and designated as AHL. In this paper, AHL extracts were added to human liver hepatocellular cells HepG-2, human gastric cancer cell SGC-7901, human breast adenocarcinoma cell MCF-7 and human umbilical vein endothelial cell EVC-304, to screen one or more AHL-sensitive tumor cell. Among these cells, HepG-2 was the most sensitive to AHL treatment, a very low dose ($0.8{\mu}g/ml$) significantly inhibiting proliferation. The non-tumor cell EVC-304, however, was not apparently affected. Effect of AHL on HepG-2 cells was then explored. We found that the AHL could cause HepG-2 cycle arrest at G2/M checkpoint, induce apoptosis, and interrupt polymerization of microtubules. In addition, expression of two cell cycle-regulated proteins, CyclinB1 and CDK1, was up-regulated upon AHL treatment. Up-regulation of the Fas, Fas ligand, Caspase-8 and Caspase-3 was observed as well, which might imply roles for the Fas/FsaL signaling pathway in the AHL-induced apoptosis of HepG-2 cells.