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Plants are the major source of therapeutic compounds and have huge applications in Pharma Industry. To identify new sources of therapeutic compounds, we studied acute toxicity, antihyperglycemic, anti-inflammatory, and anticoagulant activities of the polar and nonpolar fractions of Justicia aurea (J. aurea). Our initial phytochemical screening of J. aurea exhibited the presence of numerous secondary metabolites such as reducing sugars, glycosides, tannins, gums, alkaloids, phenolic compounds, and carbohydrates which might be primarily responsible for its medicinal properties. In the acute toxicity test, the result showed no toxicity up to 2000 mg/kg. In the antihyperglycemic activity test, administration of petroleum ether fraction and water fraction of J. aurea extract to glucoseloaded mice at 250 and 500 mg/kg body weight (BW) reduced the blood glucose levels compared to control mice. Between two fractions, the water fraction was found to exhibit better potentiality at 500 mg/kg BW. In the anti-inflammatory assay, at 250 and 500 mg/kg water fraction exhibited anti-inflammation by 20.00% and 31.67%, respectively and petroleum ether fraction by 13.33% and 18.00%, respectively. In anticoagulant activity, the test indicated that water fraction has minor anticoagulant potentiality compared to control. In conclusion, the polar water fraction shows better medicinal properties than the nonpolar petroleum ether fraction of J. aurea.

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Concomitant increase of auxin-responsive factors ARF16 and ARF17, along with enhanced expression of ARF10 in resistant Sinapis alba compared with that in susceptible Brassica juncea upon challenge with Alternaria brassicicola, revealed that abscisic acid (ABA)-auxin crosstalk is a critical factor for resistance response. Here, we induced the ABA response through conditional expression of ARF10 in B. juncea using the A. brassicicola-inducible GH3.3 promoter. Induced ABA sensitivity caused by conditional expression of ARF10 in transgenic B. juncea resulted in tolerance against A. brassicicola and led to enhanced expression of several ABA-responsive genes without affecting the auxin biosynthetic gene expression. Compared with ABI3 and ABI4, ABI5 showed maximum upregulation in the most tolerant transgenic lines upon pathogen challenge. Moreover, elevated expression of ARF10 by different means revealed a direct correlation between ARF10 expression and the induction of ABI5 protein in B. juncea. Through in vitro DNA-protein experiments and chromosome immunoprecipitation using the ARF10 antibody, we demonstrated that ARF10 interacts with the auxin-responsive elements of the ABI5 promoter. This suggests that ARF10 may function as a modulator of ABI5 to induce ABA sensitivity and mediate the resistance response against A. brassicicola.