Chronic inflammation driven by Cyclooxygenase-2 (COX-2) overexpression plays a key role in lung cancer (LC) progression, making it a critical therapeutic target. This study explores thymoquinone (TQ), a potent bioactive phytochemical derived from Nigella sativa, known for its anti-inflammatory and anti-cancer effects, focusing on its ability to suppress lipopolysaccharide (LPS)-induced COX-2 expression via microRNA hsa-miR-199a-3p modulation in LC cells. Using A549 and SHP-77 LC cells, we tested the effect of TQ under LPS stimulation and miRNA inhibition. Advanced techniques like TaqMan qPCR, luciferase reporter gene constructs, and anti-miRNA transfection confirmed that miR-199a-3p directly silences COX-2. Western blot and ELISA assays revealed that TQ dramatically reduces COX-2 protein and PGE2 levels by boosting miRNA-199a-3p. Importantly, TQ also blocked MAPK (p38, JNK, ERK) and NF-κB activation, even when miR-199a-3p was suppressed, proving its multi-targeted action beyond miRNA regulation. These findings reveal a novel anti-inflammatory mechanism, where TQ curbs COX-2-driven inflammation by enhancing miR-199a-3p, simultaneously shutting down pro-cancer MAPK/NF-κB signaling pathways. Given the strong link between chronic inflammation and LC aggressiveness, this study positions TQ as a promising therapeutic candidate, especially for inflammation-mediated lung cancer progression. Its dual ability to modulate miRNA and key signaling cascades makes it a compelling option for future LC treatment strategies.

Background and Aim: Paracetamol (PCM) ingestion is one of the most frequent global causes of toxicity. Salvadora persica L. is a plant that among many other effects exhibits potent antioxidant, anti-inflammatory, antimicrobial, and anticancer effects. In this study, we investigated the possible protective effect of S. persica aqueous extract in the PCM overdose-induced liver and kidney injury and hematological changes in a mice model. Materials and Methods: Mice were given PCM with and without S. persica pretreatment. Blood cell counts and liver and kidney function biomarkers were measured. Liver and kidney samples were histologically examined. Results: A single overdose of PCM caused significant elevations of alanine and aspartate transaminases, alkaline phosphate, bilirubin, urea, uric acid, and creatinine compared with the control group. In addition, PCM toxicity significantly lowered red blood cell count but insignificantly increased both white blood cell and platelet counts in comparison to the control mice. Pretreatment with S. persica significantly prevented PCM-induced changes in hepatic and renal biomarkers. S. persica also caused marked reversal of hematological changes. Histologically, the liver and kidney showed inflammation and necrosis after PCM treatment, which were significantly reduced in mice pretreated with S. persica. Conclusion: Taken together, S. persica significantly inhibited PCM-induced renal, hepatic, and hematological toxicity, pointing to its possible use in the treatment of liver and renal disorders.

Dysregulated microRNA-mediated control of matrix metalloproteinase-2 (MMP-2) plays a pivotal role in lung cancer (LC) progression, though the inflammatory signaling mechanisms governing its regulation remain poorly understood. This study reveals how S100A4-activated RAGE signaling modulates MMP-2 expression through microRNA-125b-5p (miR-125b-5p) in human LC cells. Potential miRNA target genes were computationally predicted using TargetScan algorithms. Functional interaction between miR-125b-5p and MMP-2 3′UTR was experimentally validated through dual-luciferase reporter assays incorporating full-length MMP-2 3′UTR sequence. Further validation was performed through transfection with miRNA inhibitors or mimics. To delineate the underlying mechanisms, key pathways were inhibited using small-molecule antagonists targeting p38-MAPK and NF-κB. Our analysis identified a conserved miR-125b-5p binding site in the MMP-2 3′UTR. In A549 cells, S100A4 induced reciprocal regulation, simultaneously upregulating MMP-2 and downregulating miR-125b-5p, with luciferase assays confirming direct targeting. Pre-miR-125b-5p transfection effectively reduced endogenous MMP-2 levels, while p38-MAPK/NF-κB activation mediated this regulation by suppressing miR-125b-5p consequently elevating MMP-2 expression. These findings were further validated in another human LC cell, SHP-77. These findings provide the first evidence demonstrating that miR-125b-5p directly regulates MMP-2 in LC, establishing S100A4-RAGE⟶p38/NF-κB⟶miR-125b-5p⟶MMP-2 axis as a novel regulatory pathway. The results position miR-125b-5p as a dual-action biomarker and therapeutic target against MMP-2-driven LC metastasis, offering new insights into critical inflammation-to-cancer connections.

There is growing interest in finding healthier meals that offer more than just nutritional benefits. Meat and meat products are consumed all over the world, so it is possible to use them as matrices to make sure that people get enough bioactive components from their food. Besides extending the meat product's shelf-life and improving its composition (by integrating antioxidant molecules), it could also help people stay healthy by lowering lipid oxidative products. In this review, we look at whether developing and eating functional meat products is a viable method for improving meat composition and stability and reducing the oxidative consequences associated with the consumption of meat intake. The inclusion of plant bioactive compounds and antioxidants in meat products should protect the composition and quality of functional meat and meat products as well as the customers' health status. The key plant components with antioxidant capabilities employed in the composition of functional meat products will be discussed in this review.

Breast cancer is the most prevalent type of malignancy among females as per the report of the World Health Organization. There are several established chemotherapeutic regimes for the clinical management of different solid cancers; however, the after-effects of these therapeutics serve as a significant limiting factor. The natural triterpenoid compound, gedunin is one of the principal phytoconstituent found in Azadirachta indica. In this study, we have investigated the anticancer potential of gedunin against human breast cancer MDA-MB-231 and MCF-7 cells. Based on computational studies, gedunin exhibited significantly higher binding affinity of −7.1 and −6.2 Kcal/mol towards Janus kinase (JAK) and STAT proteins, respectively. Further, the anticancer potential of gedunin against human breast cancer was studied using hormone-independent and -dependent MCF-7 and MDA-MB-231 cell lines, respectively. The results indicated that gedunin inhibited the growth and multiplication of both MCF-7 and MDA-MB-231 cells. The nuclear fragmentation and ROS were qualitatively enhanced in the treated MCF-7 and MDA-MB-231 cells in comparison to untreated cells. The caspase-3 level was significantly enhanced with a concomitant decline in JAK1 and STAT3 mRNA expression. Based on these results, gedunin might be considered as a potential therapeutic lead against hormone-dependent and -independent breast cancer MCF-7 and MDA-MB-231 cells, respectively. However, further detailed mechanistic studies are warranted to conclusively establish the anti-breast cancer effects.