L. (family Araliaceae) is classified as a conventional plant used as a medicinal product in the cure and prevention of upper respiratory tract inflammation and infection due to its secretolytic and broncholytic effects. Our research was conducted to authenticate the anti-inflammatory effect of ivy leaves extract in the prevention of acute lung injury (ALI) caused by intranasal administration of lipopolysaccharides (LPS). antimicrobial, anti-inflammatory, and anti-oxidant were evaluated, in addition to the acute lung inflammation model induced by LPS in mice. The animals were divided into seven groups randomly (each group containing 10 mice): control negative (saline only), control positive (LPS group), standard (Dexamethasone 2 mg/kg), ethanolic ivy leaves extract (EIE, 100 mg/kg), ethanolic ivy leaves extract (EIE, 200 mg/kg), saponin rich fraction (SRF, 100 mg/kg) and phenolic rich fraction (PRF, 100 mg/kg). Right lungs were homogenized to determine the levels of SOD, MDA, catalase, IL-10, TNF-α, NO, IL-1β, IL-6, PGE2, and MPO. Left lungs were excised for histopathology and histomorphometry. Immunohistochemistry of Cox-2 and TNF-α levels were measured. Additionally, Western blotting was used to determine the levels of phosphorylated MAPK. Also, the ethanolic extract was also standardized through HPLC analysis for its content of rutin.The data showed that the oral supplementation with EIE, 200 mg/kg significantly ( < 0.05) decreased the pro-inflammatory mediators, and oxidative stress biomarkers induced by LPS. Interestingly, the phenolics showed promising activity, therefore they are responsible for the action. In conclusion, the standardized ivy leaf extract could be advised for acute lung injury for its antimicrobial, anti-oxidant, and anti-inflammatory activities.

Biochar Magic against Abiotic Stresses - 1

Infection of mammalian cells by SARS-CoV-2 coronavirus requires primary interaction between the receptor binding domain (RBD) of the viral spike protein and the host cell surface receptor angiotensin-converting enzyme 2 (ACE2) glycoprotein. Several mutations in the RBD of SARS-CoV-2 spike protein have been reported for several variants and resulted in wide spread of the COVID pandemic. For instance, the double mutations L452R and E484Q present in the Indian B.1.617 variant have been suggested to cause evasion of the host immune response. The common RBD mutations N501Y and E484K were found to enhance the interaction with the ACE2 receptor. In the current study, we analyzed the biosynthesis and secretion of the RBD double mutants L452R and E484Q in comparison to the wild-type RBD and the individual mutations N501 and E484K in mammalian cells. Moreover, we evaluated the interaction of these variants with ACE2 by means of expression of the S protein and co-immunoprecipitation with ACE2. Our results revealed that the double RBD mutations L452R and E484Q resulted in a higher expression level and secretion of spike S1 protein than other mutations. In addition, an increased interaction of these mutant forms with ACE2 in Calu3 cells was observed. Altogether, our findings highlight the impact of continuous S1 mutations on the pathogenicity of SARS-CoV-2 and provide further biochemical evidence for the dominance and high transmissibility of the double Indian mutations.