The objective of this study was to investigate the in vitro bioactivities associated with the content of phytochemicals in the extracts from perilla seed meal extract (PSME) compared with dietary seed (PSE). PSE had higher total phenolics and flavonoids content than PSME. However, hydrophilic phytochemical contents in PSME were quantitatively equivalent to PSE. Rosmarinic acid was predominantly found in both extracts. Cell viability and anti‐mutagenicity testing demonstrated that PSE and PSME were biosecured and non‐genotoxic. Both extracts strongly scavenged free radicals and significantly reduced reactive oxygen species (ROS) production. The extracts drastically diminished nitric oxide (NO) production of LPS‐treated RAW 264.7 cells via iNOS mRNA expression. The expression of IL‐6 and COX‐2 were evidently inhibited by these extracts. It could be concluded that PSE and PSME clearly showed in vitro anti‐mutagenicity, antioxidant and anti‐inflammatory capacities. In particular, the by‐product perilla seed meal could be considered as a high nutritive functional food. Practical applications This study suggests that the seed meals, a by‐product from seed oil industry, can be utilized as a valuable dietary source for humans and animals. The high content of polyphenols and their bioactivities can be developed as functional foods, and excipients and fillers in pharmaceuticals and nutraceuticals production. Moreover, recycling of the by‐product seed meals should also reduce environmental and sanitary pollution.
In this study, the chemopreventive properties of Perilla frutescens leaf extract (PLE) on rat colon carcinogenesis were investigated during initiation and postinitiation stages. Rats were fed orally by 50 and 500 mg/kg bw of PLE continuously from 1 week before subcutaneously injection of 1,2dimethylhydrazine (DMH) until the end of experiment. PLE administration reduced the aberrant crypt foci (ACF) number in DMH-treated rats through the inhibition of hepatic cytochrome P4502E1 (CYP2E1) and bacterial b-glucuronidase activity in the colonic lumen. These events led to the reduction of DNA methylation in colonic epithelial cells. For the postinitiation model, rats were injected (s.c.) with DMH, followed by PLE administration until the end of experiment. PLE administration also reduced the ACF number in DMH-induced rats, resulting from apoptosis induction and reduction of proliferation in colon crypt cells. These studies demonstrated that perilla leaf could inhibit ACF formation and progression in DMH-initiated colon carcinogenesis in rats. Practical applicationsThis study revealed the inhibitory effect of PLE on chemical-induced colon carcinogenesis in rats.Altogether, our data supported that PLE acts as a chemopreventive agent for colon cancer. Thus, PLE might be developed as food supplement or functional tea for colon cancer prevention. K E Y W O R D S aberrant crypt foci, colon cancer, DNA methylation, functional food, perilla leaf, xenobiotic metabolism
Industrially, after the removal of oil from perilla seeds (PS) by screw-type compression, the large quantities of residual perilla seed meal (PSM) becomes non-valuable waste. Therefore, to increase the health value and price of PS and PSM, we focused on the biological effects of perilla seed oil (PSO) and rosmarinic acid-rich fraction (RA-RF) extracted from PSM for their role in preventing oxidative stress and inflammation caused by TNF-α exposure in an A549 lung adenocarcinoma culture model. The A549 cells were pretreated with PSO or RA-RF and followed by TNF-α treatment. We found that PSO and RA-RF were not toxic to TNF-α-induced A549 cells. Both extracts significantly decreased the generation of reactive oxygen species (ROS) in this cell line. The mRNA expression levels of IL-1β, IL-6, IL-8, TNF-α, and COX-2 were significantly decreased by the treatment of PSO and RA-RF. The Western blot indicated that the expression of MnSOD, FOXO1, and NF-κB and phosphorylation of JNK were also significantly diminished by PSO and RA-RF treatment. The results demonstrated that PSO and RA-RF act as antioxidants to scavenge TNF-α induced ROS levels, resulting in decreased the expression of MnSOD, FOXO1, NF-κB and JNK signaling pathway in a human lung cell culture exposed to TNF-α.
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