The demand for agricultural crops continues to escalate with the rapid growth of the population. However, extreme climates, pests and diseases, and environmental pollution pose a huge threat to agricultural food production. Silica nanoparticles (SNPs) are beneficial for plant growth and production and can be used as nanopesticides, nanoherbicides, and nanofertilizers in agriculture. This article provides a review of the absorption and transportation of SNPs in plants, as well as their role and mechanisms in promoting plant growth and enhancing plant resistance against biotic and abiotic stresses. In general, SNPs induce plant resistance against stress factors by strengthening the physical barrier, improving plant photosynthesis, activating defensive enzyme activity, increasing anti-stress compounds, and activating the expression of defense-related genes. The effect of SNPs on plants stress is related to the physical and chemical properties (e.g., particle size and surface charge) of SNPs, soil, and stress type. Future research needs to focus on the “SNPs–plant–soil–microorganism” system by using omics and the in-depth study of the molecular mechanisms of SNPs-mediated plant resistance.
Cancer is the second leading cause of death globally. Millions of persons die due to cancer each year. In the last two decades, the anticancer effects of natural flavonoids have become a hot topic in many laboratories. Meanwhile, flavonoids, of which over 8000 molecules are known to date, are potential candidates for the discovery of anticancer drugs. The current review summarizes the major flavonoid classes of anticancer efficacy and discusses the potential anti-cancer mechanisms through inflammation and oxidative stress action, which were based on database and clinical studies within the past years. The results showed that flavonoids could regulate the inflammatory response and oxidative stress of tumor through some anti-inflammatory mechanisms such as NF-κB, so as to realize the anti-tumor effect.
Our previous study showed that wedelolactone, a compound isolated from Ecliptae herba, has the potential to enhance osteoblastogenesis. However, the molecular mechanisms by which wedelolactone promoted osteoblastogenesis from bone marrow mesenchymal stem cells (BMSCs) remain largely unknown. In this study, treatment with wedelolactone (2 μg/mL) for 3, 6, and 9 days resulted in an increase in phosphorylation of extracellular signal-regulated kinases (ERKs), c-Jun N-terminal protein kinase (JNK), and p38. Phosphorylation of mitogen-activated protein kinases (MAPKs), ERK and JNK started to increase on day 3 of treatment, and p38 phosphorylation was increased by day 6 of treatment. Expression of bone morphogenetic protein (BMP2) mRNA and phosphorylation of Smad1/5/8 was enhanced after treatment of cells with wedelolactone for 6 and 9 days. The addition of the JNK inhibitor SP600125, ERK inhibitor PD98059, and p38 inhibitor SB203580 suppressed wedelolactone-induced alkaline-phosphatase activity, bone mineralization, and osteoblastogenesis-related marker genes including Runx2, Bglap, and Sp7. Increased expression of BMP2 mRNA and Smad1/5/8 phosphorylation was blocked by SP600125 and PD98059, but not by SB203580. These results suggested that wedelolactone enhanced osteoblastogenesis through induction of JNK- and ERK-mediated BMP2 expression and Smad1/5/8 phosphorylation.
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