Comprehensive biochemical approach for understanding the interaction between host "common bean" and pathogen "Colletotrichum lindemuthianum" causing bean anthracnose.

Anthracnose (ANT) caused by Colletotrichum lindemuthianum is the most devastating seed-borne fungal disease of common bean. In response to fungal infections, it is hypothesized that pathogen-plant interactions typically cause hypersensitive reactions by producing reactive oxygen species, hydrogen peroxide and lipid peroxidation of cell membranes. esent study was conducted by inoculating susceptible bean genotype "SB174" and resistant bean genotype "E10" with pathogen "C. lindemuthianum". Defense-related enzymes (ascorbate peroxidase, peroxidase, lipid peroxidase, and catalase) and C-based compounds (total phenols and flavonoids) were studied using the detached bean leaf method. Comparative defense response was studied in different plant tissues (pod, stem, and seed) in susceptible and resistant bean genotypes under uninoculated and pathogen-inoculated conditions. The host‒pathogen interaction was studied at mock inoculation, 2, 4 and 6 days after inoculation (dai). Comparing the pathogen-inoculated bean leaves to water-treated bean leaves, defense enzymes as well as total phenols and flavonoids exhibited differential expression. In a comparative study, the enzyme activity also displayed differential biochemical responses in pods, stems and seeds in both contrasting genotypes. For example, 5.1-fold (pod), 1.5-fold (stem) and 1.06-fold (seed) increases in ascorbate peroxidase activity were observed in the susceptible genotype at 6 dai compared to mock inoculation. Similarly, catalase activity in pods was upregulated (1.47-fold) in the resistant genotype and downregulated (1.30-fold) in the susceptible genotype at 6 dai. The study revealed that defense-related antioxidative enzymes, phenols and flavonoids are fine-tuned to detoxify important reactive oxygen species (ROS) molecules, induce systemic resistance and are successfully controlled in common bean plants against pathogen invasion.

Plant flavone Chrysin as an emerging histone deacetylase inhibitor for prosperous epigenetic-based anticancer therapy.

Aberrations in epigenetic mechanisms provide a fertile platform for tumour initiation and progression. Thus, agents capable of modulating the epigenetic environment of neoplasms will be a valuable addition to the anticancer therapeutics. Flavones are emerging as befitting anticancer agents due to their inherent antioxidant activity and the ability to restrain epi-targets namely histone deacetylases (HDACs). HDACs have broader implications in pathogenesis of various cancers. Chrysin, a flavone possessing the ability to inhibit HDACs could prove as a potential anticancer drug. Thus, in this article we focussed on Chrysin and its distinct antineoplastic effect against bellicose malignancies including lung, colorectal, cervical, gastric, melanoma, hepatocellular carcinoma and breast cancer. The underlying signalling cascades triggered by Chrysin for inducing cytotoxic effect in these cancer models are discussed. Importantly, approaches towards combinatorial treatments by Chrysin and commercial anticancer agents are taken into account. The downstream molecular mechanism aroused by combined therapy for abrogating onerous cancer chemoresistance is delineated as well. Moreover, the nano-combinatorial approach involving co-encapsulation of Chrysin with other herbal and non-herbal agents for clinical excellence is elucidated.

Anticancer activity of the plant flavonoid luteolin against preclinical models of various cancers and insights on different signalling mechanisms modulated.

Various signaling mechanisms contribute significantly to the development of multiple cancers. Small molecules with the potential of influencing a wide variety of molecular targets may prove as broad-spectrum anticancer agents. Flavonoids from plant sources are strongly emerging as promising antineoplastic molecules because of their ability to hamper different cancer-driving signaling pathways. Further, these flavonoids offer an additional benefit due to their congenital antioxidant potential. This paper discusses the anticancer activity of luteolin against a number of cancers including leukemias, prostate cancer, pancreatic cancer, breast cancer, lung cancer, colorectal cancer, melanoma, liver, gastric, and brain cancer. Strong emphasis has been laid on key molecular mechanisms impacted by luteolin for exerting antineoplastic effect. Importantly, certain epigenetic targets like histone deacetylases (HDACs), DNA methylation regulator enzymes that are influenced by this befitting flavone for inducing cytotoxicity in certain preclinical cancer models, have also been made the part of this review. Additionally, the significantly improved therapeutic benefits of luteolin in combination with other therapeutics are comprehensively discussed. The current loopholes in luteolin research are also considered, which may open novel routes for further valuable studies on this promising flavone.