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Simple Summary: Gastric cancer (GC) ranks as one of the most life-threatening malignancies worldwide, and over one billion new cases and 783,000 deaths were reported last year. The incidence of GC is exceptionally high in Asian countries. Multiple oncogenic signaling pathways are aberrantly activated and implicated in gastric carcinogenesis, leading to the malignant phenotype acquisition. G-protein-coupled receptor (GPCR) signaling is one of them, and the aberrant activation of GPCRs and G proteins promotes GC progression. The activated GPCRs/G proteins might serve as useful biomarkers for early diagnosis, prognostic prediction, and even clinically therapeutic targets. This review summarized the recent research progress of GPCRs and highlighted their mechanisms in tumorigenesis, especially in GC initiation and progression. G-protein-coupled receptors (GPCRs) belong to a cell surface receptor superfamily responding to a wide range of external signals. The binding of extracellular ligands to GPCRs activates a heterotrimeric G protein and triggers the production of numerous secondary messengers, which transduce the extracellular signals into cellular responses. GPCR signaling is crucial and imperative for maintaining normal tissue homeostasis. High-throughput sequencing analyses revealed the occurrence of the genetic aberrations of GPCRs and G proteins in multiple malignancies. The altered GPCRs/G proteins serve as valuable biomarkers for early diagnosis, prognostic prediction, and pharmacological targets. Furthermore, the dysregulation of GPCR signaling contributes to tumor initiation and development. In this review, we have summarized the research progress of GPCRs and highlighted their mechanisms in gastric cancer (GC). The aberrant activation of GPCRs promotes GC cell proliferation and metastasis, remodels the tumor microenvironment, and boosts immune escape. Through deep investigation, novel therapeutic strategies for targeting GPCR activation have been developed, and the final aim is to eliminate GPCR-driven gastric carcinogenesis. [ABSTRACT FROM AUTHOR]

A new heterometallic coordination polymer [CuNa(ehbd)2(dca)(CH3OH)]n(1) (Hehbdis 3-ethoxy-2-hydroxybenzaldehyde,dcais N(CN)2−) has been synthesized under room temperature and structurally characterized by elemental analysis, IR, UV-Vis, and single-crystal X-ray diffraction. Complex1is axisymmetric heterobinuclear copper-sodium complex. The geometry around copper atom can be described as slightly distorted tetragonal pyramid geometry, and sodium can be described as slightly distorted octahedral geometry. Complex1further constructed 1-D chain through μ1,5-dcabridging. Luminescent property of1has also been studied. [ABSTRACT FROM AUTHOR]

Objective: To investigate the protective effect of quercetin on radiation induced lung injury (RILI) and related mechanisms., Materials and Methods: Mice treated with radiation and/or quercetin were sacrificed at 1-8 weeks after irradiation under anesthesia. Lung tissues were collected for histological examination. Immunohistochemistry (IHC) and Western blotting were performed to detect the protein expression of nuclear factor-κB (NF-κB) and Mitogen-activated protein kinases (MAPK) pathway., Results: Hematoxylin and eosin (HE) staining showed that radiation controls displayed more severe lung damage than quercetin groups, either high or low dose. Results of IHC and Western blotting demonstrated the expression level of NF-κB to be decreased and that of an inhibitor of NF-κB (Iκb-α) to be increased by the quercetin intervention compared with the radiation control group. Numbers of JNK/SAPK, p38 and p44/p42 positive inflammatory cells were decreased in the radiation+quercetin injection group (P<0.05)., Conclusions: Quercetin may play a radio-protective role in mice lung via suppression of NF-κB and MAPK pathways.