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In recent years, introducing electrospun airfilters to enhance the removal of PM2.5 and PM10–2.5 has received much interest. In this study, a novel poly-(vinyl) alcohol (PVA)/carbon nanoparticle (CNP)/tea leaf extract (TLE), functionalized nanofibrous air filter (FNA) was fabricated using an electrospinning method. Novelty of the unique work in the blending of CNP and TLE, first of its kind, for the preparation of FNA. Polysaccharide crosslinked FNA has a carbon complex with two monosaccharide units to produce the intrinsic properties of the PM2.5 and PM10–2.5 removal efficiency. The FNA had promising traits of UV protection. The prepared FNA was characterized using physicochemical, mechanical, antimicrobial activity, etc., in addition to its PM2.5 and PM10–2.5 removal efficiency. Pore size and distribution study using the capillary flow porometry method has proved the structure of FNA. FNA exhibited excellent low pressure drop (110 Pa), which are promising characteristics for air purification. FNA from PVA: CNP: TLE exhibited high PM2.5 and PM10–2.5 removal efficiencies of 99.25% and 99.29%, respectively. Hence, the study proved.

Colorectal cancer is one of the most leading death-causing cancers in the world. Vernodalin, a cytotoxic sesquiterpene, has been reported to possess anticancer properties against human breast cancer cells. We aimed to examine the anticancer mechanism of vernodalin on human colon cancer cells. Vernodalin was used on human colon cancer cells, HT-29 and HCT116. The cytotoxicity of vernodalin on human colon cancer cells was determined through in vitro 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay. Small interfering RNA was used to analyze the cascade activation of mitogen-activated protein kinase (MAPK) pathway, c-Jun N-terminal kinase (JNK) in HT-29, and HCT116 cells against vernodalin treatment. The protein expressions of caspase 3, Bcl-2, and Bax were examined through Western blot analysis. Immunoblot analysis on the JNK, ERK, and p38 MAPK pathways showed increased activation due to vernodalin treatment. It was proven from the JNK and p38 inhibition test that both pathways are significantly activated by vernodalin to induce apoptosis. Our results, collectively, showed the apoptosis-induced anticancer mechanism of vernodalin on human colon cancer cells that was mediated through the activation of JNK pathway and apoptotic regulator proteins. These results suggest that vernodalin could be developed as a potent chemotherapeutic agent for human colorectal cancer treatment.

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