Cinnamon for your lungs

Drink cinnamon tea to protect your lungs.
Research:
Identification of novel Nrf2 activators from Cinnamomum chartophyllum H.W. Li and their potential application of preventing oxidative insults in human lung epithelial cells
Cumulative evidences have proved that Nrf2 is highly expressed in relative abundance in human lung tissue, to counteract the insults caused by environmental oxidants and toxicants [31]. Plenty of Nrf2 inducers, exemplified by SF, resveratrol, xanthohumol, tanshinone I, bis[2-hydroxybenzylidene]acetone, have demonstrated protective and therapeutic effects on lung disorders [10][17][32][33][34]. Nrf2 is a good target for discovering agents possessing therapeutic effect on human lung diseases [35][36][37]. In this study, experiments in vitro were performed using Beas-2B cells to evaluate the Nrf2 inducing effect of NLD and THD on human normal lung tissue. We have found that NLD and THD significantly activated Nrf2 and its downstream genes, NQO1, and γ-GCS, and enhanced the nuclear translocation and stabilization of Nrf2 in human lung epithelial Beas-2B cells (Fig. 3). According to these data, NLD and THD are verified to be canonical Nrf2 activators. More importantly, NLD and THD had no toxicity under the Nrf2 inducing doses in Beas-2B cells, and hada broad effective dose range (Fig. 3A and S2). Furthermore, NLD and THD-mediated Nrf2 activations in Beas-2B cells are intermittent (Fig. 3B), which are similar to that of chemopreventive agents (e.g. SF), but different from that of toxicants and carcinogens [38]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5608562/

Abstract

Human lung tissue, directly exposed to the environmental oxidants and toxicants, is apt to be harmed to bring about acute or chronic oxidative insults. The nuclear factor erythroid 2-related factor 2 (Nrf2) represents a central cellular defense mechanism, and is a target for developing agents against oxidative insult-induced human lung diseases. Our previous study found that the EtOH extract of Cinnamomum chartophyllum protected human bronchial epithelial cells against oxidative insults via Nrf2 activation. In this study, a systemic phytochemical investigation of the aerial parts of C. chartophyllum led to the isolation of thirty chemical constituents, which were further evaluated for their Nrf2 inducing potential using NAD(P)H: quinone reductase (QR) assay. Among these purified constituents, a sesquiterpenoid bearing α, β-unsaturated ketone group, 3S-(+)-9-oxonerolidol (NLD), and a diphenyl sharing phenolic groups, 3, 3′, 4, 4′-tetrahydroxydiphenyl (THD) significantly activated Nrf2 and its downstream genes, NAD(P)H quinone oxidoreductase 1 (NQO-1), and γ-glutamyl cysteine synthetase (γ-GCS), and enhanced the nuclear translocation and stabilization of Nrf2 in human lung epithelial cells. Importantly, NLD and THD had no toxicities under the Nrf2 inducing doses. THD also demonstrated a potential of interrupting Nrf2-Keap1 protein-protein interaction (PPI). Furthermore, NLD and THD protected human lung epithelial cells against sodium arsenite [As(III)]-induced cytotoxicity. Taken together, we conclude that NLD and THD are two novel Nrf2 activators with potential application of preventing acute and chronic oxidative insults in human lung tissue. https://www.ncbi.nlm.nih.gov/pubmed/28942193