Electronic cigarettes (e-cigarettes) are becoming increasingly popular worldwide and their cellular effects warrant further evaluation. In this study, we investigated the effects of an e-cigarette cartridge solution on allergen related asthmatic airway inflammation (AI) and airway hyperresponsiveness (AHR), when it is delivered by intratracheal route in mice. Asthmatic AI and AHR were induced by systemic sensitization to ovalbumin (OVA) followed by intratracheal, intraperitoneal, and aerosol allergen challenges in BALB/c mice. The cartridge solution of e-cigarette (containing 16 mg/ml nicotine) was diluted 50 times and 100 μl of the diluted solution was intratracheally instilled to OVA-sensitized (OVA-S) mice two times a week for 10 weeks. Long-term e-cigarette inhalation elicited no remarkable changes in the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase enzymes in serum, however, increased infiltration of inflammatory cells including eosinophils, into airways from blood, aggravated the asthmatic AI and AHR, and stimulated the production of cytokines such as interleukin (IL)-4, IL-5 and IL-13, and OVA-specific IgE production. Our data suggest that the inhalation of e-cigarette solutions can function as an important factor to exacerbate the allergy-induced asthma symptoms. Further studies are needed to address the effects of e-cigarette solutions on human health.
Cold stress is known as the important yield-limiting factor of heading type Kimchi cabbage (HtKc, Brassica rapa L. ssp. pekinensis), which is an economically important crop worldwide. However, the biochemical and molecular responses to cold stress in HtKc are largely unknown. In this study, we conducted transcriptome analyses on HtKc grown under normal versus cold conditions to investigate the molecular mechanism underlying HtKc responses to cold stress. A total of 2131 genes (936 up-regulated and 1195 down-regulated) were identified as differentially expressed genes and were significantly annotated in the category of “response to stimulus”. In addition, cold stress caused the accumulation of polyphenolic compounds, including p-coumaric, ferulic, and sinapic acids, in HtKc by inducing the phenylpropanoid pathway. The results of the chemical-based antioxidant assay indicated that the cold-induced polyphenolic compounds improved the free-radical scavenging activity and antioxidant capacity, suggesting that the phenylpropanoid pathway induced by cold stress contributes to resistance to cold-induced reactive oxygen species in HtKc. Taken together, our results will serve as an important base to improve the cold tolerance in plants via enhancing the antioxidant machinery.
This study aimed to evaluate the effects of taxifolin and sorghum ethanol extract on free fatty acid (FFA)-induced hepatic insulin resistance. FFA treatment decreased glucose uptake by 16.2% compared with that in the control, whereas taxifolin and sorghum ethanol extract increased the glucose uptake. Additionally, taxifolin and sorghum ethanol extract increased the expression of p-PI3K, p-IRS1, p-AKT, p-AMPK, and p-ACC in FFA-induced hepatocytes. Furthermore, FFA treatment increased the expression of miR-195. However, compared with the FFA treatment, treatment with taxifolin and sorghum ethanol extract decreased miR-195 expression in a dose-dependent manner. Taxifolin and sorghum ethanol extract enhanced p-IRS1, p-PI3K, p-AMPK, p-AKT, and p-ACC expression by suppressing miR-195 levels in miR-195 mimic- or inhibitor-transfected cells. These results indicate that taxifolin and sorghum ethanol extract attenuate insulin resistance by regulating miR-195 expression, which suggests that taxifolin and sorghum ethanol extract may be useful antidiabetic agents.
Owing to the increase in price of cigarettes in Korea, herbal cigarettes have received increasing attention as a non-smoking aid; however, its safety has hardly been studied. We analyzed some of the toxic components in the mainstream smoke of herbal cigarettes, performed a mutagenicity test on smoke condensates for safety assessment, and compared the results with the corresponding values of a general cigarette with the same tar content. Herbal cigarette “A” was smoked using automatic smoking machine under ISO conditions in a manner similar to general cigarette “T”. The tar content measured was higher than that inscribed on the outside of a package. The mainstream smoke of herbal cigarette “A” did not contain detectable levels of tobacco-specific nitrosamines and nicotine. Carbon monoxide and benzo(α)pyrene contents in herbal cigarette “A” were higher than those in the general cigarette “T”. The phenolic contents such as hydroquinone, resorcinol, and catechol in herbal cigarette “A” were higher than those in the general cigarette “T”, but cresol contents in herbal cigarette “A” were lower than those in the general cigarette “T”. The content of aromatic amines such as 4-aminobiphenyl in herbal cigarette “A” was higher than that in the general cigarette “T”; however, this difference was not statistically significant. On the other hand, 1-aminonaphthalene, 2-aminonaphthalene, and 3-aminobiphenyl contents in herbal cigarette “A” were lower than those in the general cigarette “T”. The smoke condensates of herbal cigarette “A” exhibited a higher mutagenic potential than the condensates from the general cigarette “T” at the same concentration. We concluded that the mainstream smoke of herbal cigarette contains some toxic components, the smoke condensates of herbal cigarettes are mutagenic similar to general cigarette because of combustion products, and that the evaluation of the chemical and biological safety of all types of herbal cigarettes available on the market.