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Epstein–Barr Virus and Treatment of Its Infection
Published in Satya Prakash Gupta, Cancer-Causing Viruses and Their Inhibitors, 2014
Tarun Jha, Amit Kumar Halder, Nilanjan Adhikari
Some clauslactones were isolated from the leaves of Clausena excavate belonging to the family Rutaceae by Ito et al. (2000a). Among these, clauslactone C (94, Figure 6.11) was observed to be the most potent compound. Carbazole alkaloids were also isolated by Ito et al. (2000b) from Clausena anisata belonging to the family Rutaceae. One compound—ekeberginine (95, Figure 6.11)—was found to be the most potent while others also showed potent inhibitory activity against EBV-EA activation. Compound 96 (Figure 6.11) was found to be the most potent depsidone from Garcinia assigu (family: Guttiferae) (Ito et al. 2001). Tamura et al. (2002) synthesized seven shinjulactone C (quassinoid isolated from Ailanthus altissima) derivatives and evaluated their antitumor-promoting effects against EBV-EA. Among these synthetic derivatives, compound 97 (Figure 6.11), having a 3′, 3′-dimethylsuccinate moiety, showed the highest inhibition. A SAR study suggested that succinate derivatives have better activity than glutarates. Some diterpene compounds were isolated from the cones of Pinus luchuensis (family: Pinaceae) by Minami et al. (2002), and 15-nor-14-oxolabda-8(17)-12E-dien-19-oic acid (98, Figure 6.11) exhibited the highest activity. Some sarcophine analogs were also tested against EBV-EA by Katsuyama et al. (2002) where some compounds showed higher chemopreventive activity; the highest activity was associated with 99 (Figure 6.11). Some xanthones were isolated from the stem bark of Calophyllum brasilienses (family: Guttiferae) by Ito et al. (2002). Some of these compounds showed promising inhibitory activity against TPA-induced EBV-EA activation in Raji cells, and brasixanthone B (100, Figure 6.11) was found to be the most potent.
Therapeutic potentials of endophytes for healthcare sustainability
Published in Egyptian Journal of Basic and Applied Sciences, 2021
Ayodeji O. Falade, Kayode E. Adewole, Temitope C. Ekundayo
Other compounds of endophytic sources, which have displayed anti-inflammatory activity in vitro include cowabenzophenone A from Aspergillus terreus residing in Bruguiera gymnorrhyza, desmethyldichlorodiaportintone from an Ascomycota species hosted by Pluchea indica [49,50] and terrusnolide A, B, C, and D isolated from Aspergillus species hosted by Tripterygium wilfordii [51]. Others include corynesidone A, C, and D and corynether A isolated from Corynespora cassicola, which caused concentration-dependent reduction of ‘LPS-induced TNF-α and iNO in RAW264.7’ cells [52]. It is worthy of note that majority of the listed (Table 1) endophytic bioactive compounds with anti-inflammatory activities belong to the following classes: depsidoenes, butenolides, maleimide-bearing compounds, ergosterol, spirobisnaphthalenes, depsidones and benzopyran derivatives.
Lichenochemicals: extraction, purification, characterization, and application as potential anticancer agents
Published in Expert Opinion on Drug Discovery, 2020
Mahshid Mohammadi, Vasudeo Zambare, Ladislav Malek, Christine Gottardo, Zacharias Suntres, Lew Christopher
Caski and HeLa cervical carcinoma cell lines have been challenged with extracts and lichenochemicals from various lichen species (Table 8). Death of cervical cancerous cells was caused by apoptosis due to proliferation inhibition of 2-hydroxy-4-methoxy 3,6 dimethylbenzoic acid, as evidenced from the cell morphology, i.e. nuclear shrinkage and chromatin condensation [114].The secondary depsidone metabolite pysodic acid from H. physodes remarkably decreased viability and proliferation of HeLa cells [160]. Purified protolichesterinic acid had a pro-apoptotic effect, activated caspase-3, 8 and 9 and increased cytotoxicity alone and in combination with doxorubicin after 24 h of exposure to HeLa cells [161]. Lobaric acid and lobarstin from the antarctic lichen Stereocaulon alpnum demonstrated apoptosis by down-regulation of Bcl-2, upregulation of PARP, and cell cycle arrest at G2 phase [155].