The role of vasoactive intestinal peptide in pulmonary diseases.

Vasoactive intestinal peptide (VIP) is an abundant neurotransmitter in the lungs and other organs. Its discovery dates back to 1970. And VIP gains attention again due to the potential application in COVID-19 after a research wave in the 1980s and 1990s. The diverse biological impacts of VIP extend beyond its usage in COVID-19 treatment, encompassing its involvement in various pulmonary and systemic disorders. This review centers on the function of VIP in various lung diseases, such as pulmonary arterial hypertension, chronic obstructive pulmonary disease, asthma, cystic fibrosis, acute lung injury/acute respiratory distress syndrome, pulmonary fibrosis, and lung tumors. This review also outlines two main limitations of VIP as a potential medication and gathers information on extended-release formulations and VIP analogues.

Dietary pattern interfered with the impacts of pesticide exposure by regulating the bioavailability and gut microbiota.

Dietary intake is an essential way for pesticides to enter the human body. The effects of dietary pattern on the risks of pesticides and what diet can reduce the damage are largely unknown. Here, it is found that Mediterranean diet and Vegetarian diet could alleviate insulin resistance and obesity induced by chlorpyrifos, while Western diet could aggravate that. Gut microbiota and chlorpyrifos bioavailability mediated by the diets were involved in these effects. Both the dietary pattern and chlorpyrifos could change the composition of gut microbiota. Chlorpyrifos caused gut dysbacteriosis which was an important reason for the induced metabolic syndrome. Mediterranean diet and Vegetarian diet could maintain gut microbiota homeostasis and increase intestinal bacteria producing short-chain fatty acids, repair the gut microbiota and intestinal barrier damaged by chlorpyrifos. High dietary fat intake increased the bioavailability of chlorpyrifos, which aggravated the gut dysbacteriosis and destruction of intestinal integrity. Thus, the amount of endotoxin entering the blood increased and caused low-grade inflammation, which was also an important pathway of metabolic syndrome. The results suggested that although it was almost impossible to avoid the exposure to pesticides in modern life, healthy diets could regulate beneficial gut microbiota and alleviate the risk of pesticide exposure.

Dasatinib inhibits c-src phosphorylation and prevents the proliferation of Triple-Negative Breast Cancer (TNBC) cells which overexpress Syndecan-Binding Protein (SDCBP).

Triple negative breast cancer (TNBC) progresses rapidly but lacks effective targeted therapies. Our previous study showed that downregulating syndecan-binding protein (SDCBP) in TNBC inhibits the proliferation of TNBC cells. Dasatinib is a new small-molecule inhibitor of c-src phosphorylation. The aim of this study was to investigate if SDCBP is a potential marker to indicate whether a TNBC is suitable for dasatinib therapy. This study applied co-immunoprecipitation to identify the interaction between SDCBP and c-src in TNBC cell lines. In addition, immunohistochemistry was used to investigate SDCBP and tyrosine-419 phosphorylated c-src (p-c-src-Y419) expression in TNBC tissues. SDCBP-overexpressing MDA-MB-231 cells were then constructed to evaluate the effects of dasatinib on SDCBP-induced TNBC progression in vitro and tumor formation in nude mice. We found wild-type SDCBP interacted with c-src and promoted the phosphorylation of c-src; this phosphorylation was completely blocked by dasatinib. SDCBP lacking the PDZ domain had no such effect. Among the 52 consecutive random TNBC cases examined, the expression of SDCBP was consistent with that of p-c-src-Y419, and positively correlated with histological grading or Ki-67 levels. SDCBP overexpression significantly accelerated the proliferation and cell cycle progression of the TNBC cell line MDA-MB-231; these effects were prevented by dasatinib treatment. However, the subsequent inhibition of p27 expression partially restored the proliferation and viability of the TNBC cells. The results of this study suggest that SDCBP interacts with c-src, regulates G1/S in TNBC cells, and enhances tumor cell proliferation by promoting the tyrosine phosphorylation of c-src at residue 419. Dasatinib inhibits such phosphorylation and blocks SDCBP-induced cell cycle progression. Therefore, SDCBP might be an important marker for identifying TNBC cases that are suitable for dasatinib therapy.

Ferrocenyl-substituted curcumin: can it influence antioxidant ability to protect DNA?

The antioxidant capacities of ferrocenyl-substituted curcumin derivatives including 1,7-bis(p-hydroxy-m-methoxyphenyl)-4-ferrocenylidene-hepta-1,6-diene-3,5-dione (FCU), 1-(p-hydroxy-m-methoxyphenyl)-3-hydroxy-7-ferrocenyl-hepta-1,4,6-trien-5-one (FFT), and 1-(p-hydroxy-m-methoxyphenyl)-5-ferrocenyl-penta-1,4-dien-3-one (FDZ) were evaluated in 2,2'-azobis(2-amidinopropane hydrochloride) (AAPH), Cu2+/glutathione (GSH), and hydroxyl radical (.OH)-induced oxidation of DNA, and in trapping 2,2'-diphenyl-1-picrylhydrazyl (DPPH), 2,2'-azinobis(3-ethylbenzothiazoline-6-sulfonate) cationic radical (ABTS+), and galvinoxyl radicals. FCU, FFT, and FDZ protected DNA against Cu2+/GSH-induced oxidation, but promoted .OH-induced oxidation of DNA. FCU, FFT, and FDZ scavenged 9.5, 5.7, and 4.7 radicals in protecting DNA against AAPH-induced oxidation. FCU can trap more DPPH and ABTS+ than FDZ and FFT, whereas FCU, FFT, and FDZ cannot react with galvinoxyl radical. Both phenolic hydroxyl groups and iron atom in ferrocenylidene curcumin derivatives play antioxidant role in this case.