Author: Rodrigues, Maria A. ; Da Silva, José Paulo ; Gama, Florinda ; Pestana, Maribela ; Rodrigues, Maria A ; Saavedra, Teresa ; de Varennes, Amarilis ; Correia, Pedro José

Iron (Fe) chlorosis is very common in plants cultivated in calcareous soils of the Mediterranean basin and is usually corrected by the application of Fe chelates to the soil, which can have a negative impact on the environment. The aim of this experiment was to assess the role of quercetin, a natural compound widely present in plants and known to bind Fe, in correcting Fe chlorosis when supplied in the Hoagland nutrient solution. In this context, strawberry plants were grown at different Fe concentrations, with 0 (Fe0), 1 (Fe1) and 5 (Fe5) μM of Fe in the nutrient solution, until the onset of clear Fe chlorosis symptoms. Subsequently, the recovery of Fe chlorosis was investigated through the addition of Fe and/or quercetin (Q) to nutrient solutions. Throughout the experiment, leaf chlorophyll (Chl) was estimated using the SPAD values. The root ferric chelate-reductase (FCR) activity was determined in the root apices, and the foliar Fe concentration was also quantified. At the end of the experiment, plants grown without Fe but supplemented with Fe1 plus quercetin [Fe0+(Fe1+Q)] recovered completely from Fe chlorosis and showed a Chl concentration (700-800 μmol m^-2) in young leaves similar to that observed in control plants (Fe5). The remaining treatments exhibited lower Chl concentrations, with values ranging from 92.4 to 217.0 μmol of Chl per m². FCR activity was approximately five-to six-fold higher in the Fe0+(Fe1+Q) treatment than in the Fe0 and Fe5 treatments. However, the plants that were consistently grown with Fe in the nutrient solution (Fe1 and Fe5) exhibited the highest Fe content in their leaves. The findings suggest that quercetin has the potential to function as an Fe complexing agent, thereby enhancing the recovery of strawberry plants with Fe deficiency.

01 Sep 2024·The Spine Journal

Senolytics cocktail dasatinib and quercetin alleviate chondrocyte senescence and facet joint osteoarthritis in mice

Article

Author: Duan, Chunyue ; Zhao, Jinyun ; Sun, Yi ; He, Rundong ; Zheng, Lifu ; Liu, Zhide ; Hu, Jianzhong ; Duan, Chunyue ; Wu, Tianding ; Hu, Jianzhong ; Dai, Guoyu ; Cao, Yong ; Jin, Yuxin

BACKGROUND CONTEXTLow back pain (LBP) is a pervasive issue, causing substantial economic burden and physical distress worldwide. Facet joint osteoarthritis (FJ OA) is believed to be a significant contributor to this problem. However, the precise role of chondrocyte senescence in FJ OA remains unclear, as does whether the clearance of chondrocyte senescence can alleviate the progression of FJ OA.PURPOSEThe goal of this study was to understand the potential of Dasatinib (D) and Quercetin (Q) as a treatment to clear chondrocyte senescence during the progression of FJ OA.STUDY DESIGNWe used a preclinical bipedal standing mice model with the administration of Dasatinib (D) (5 mg/kg) and Quercetin (Q) (50 mg/kg) after 10 weeks of bipedal standing.MATERIALS AND METHODSHuman degenerative lumbar facet joint (LFJ) samples were obtained to investigate the relationship between chondrocyte cellular senescence and LFJ osteoarthritis (OA). Subsequently, we established an in vitro model of excessive mechanical stress on chondrocytes and an in vivo bipedal standing mice model to induce LFJ OA. IHC (immunohistochemistry) staining in vivo and SA-β-gal staining, qRT-PCR and Western blot analysis were applied to test the senolytic effect of the combination of Dasatinib (D) and Quercetin (Q). IHC staining and X-ray microscope were also performed to examine the contribution of D+Q to the anabolism in cartilage and subchondral bone recoupling. Immunofluorescence and Western blot analysis in vitro and IHC staining in vivo were conducted to assess the impact of D+Q on the regulation of the NF-κB pathway activation during chondrocyte senescence.RESULTSWe observed that facet joint cartilage degeneration is associated with chondrocyte cellular senescence in both human and mouse degenerative samples. Following treatment with D+Q in vitro, cellular senescence was significantly reduced. Upon oral gavage administration of D+Q in the bipedal standing mice model, decreased cellular senescence and reversed chondrocyte anabolism were observed. Furthermore, administration of D+Q maintained subchondral bone remodeling homeostasis and potentially reversed the activation of the NF-κB pathway in chondrocytes of the lumbar facet joint.CONCLUSIONSIn summary, our investigation unveiled a significant correlation between chondrocyte senescence and LFJOA. Treatment with the senolytic combination of D+Q in FJ OA yielded a notable reduction in chondrocyte senescence, along with a decrease in the release of SASP factors. Additionally, it facilitated the promotion of cartilage anabolism, maintenance of subchondral bone coupling, and amelioration of NF-κB pathway activation.CLINICAL SIGNIFICANCEOur outcomes revealed that D+Q, the renowned combination used for senolytic treatment, alleviate the progression of LFJ OA. The utilization of D+Q as a senolytic demonstrates a novel and promising alternative for LFJ OA treatment.

01 Jan 2024·Current Research in Pharmacology and Drug Discovery

Quercetin prevents rats from type 1 diabetic liver damage by inhibiting TGF-ꞵ/apelin gene expression

Article

Author: Firouzeh, Gholampour ; Zeinab, Karimi ; Susan, Abbasi

BackgroundHyperglycemia-induced oxidative stress is a significant contributor to diabetic complications, including hepatopathy. The current survey aimed to evaluate the ameliorative effect of quercetin (Q) on liver functional disorders and tissue damage developed by diabetes mellitus in rats.MethodsGrouping of 35 male Wistar rats was performed as follows: sham; sham + quercetin (sham + Q: quercetin, 50 mg/kg/day in 1 ml 1% DMSO for 6 weeks, by gavage); diabetic control (Diabetes: streptozotocin (STZ), 65 mg/kg, i.p.); diabetic + quercetin 1 (D + Q1: quercetin, 25 mg/kg/day in 1 ml 1% DMSO for 6 weeks, by gavage after STZ injection); and diabetic + quercetin 2 (D + Q2: quercetin, 50 mg/kg/day in 1 ml 1% DMSO for 6 weeks, by gavage after STZ injection). Body weight, food intake, and water intake were measured. Ultimately, the samples of plasma and urine, as well as tissue samples of the liver and pancreas were gathered for later assays.ResultsSTZ injection ended in elevated plasma blood glucose levels, decreased plasma insulin levels, liver dysfunction (increased activity levels of AST, ALT, and ALP, increased plasma levels of total bilirubin, cholesterol, LDL, triglyceride, decreased plasma levels of total protein, albumin and HDL), enhanced levels of malondialdehyde, diminished activities of antioxidant enzymes (superoxide dismutase, and catalase), reduced level of glutathione (GSH) increased gene expression levels of apelin and TGF-ꞵ, plus liver histological destruction. All these changes were diminished by quercetin. However, the measure of improvement in the D + Q2 group was higher than that of the D + Q1 group.ConclusionsQuercetin improved liver function after diabetes mellitus type 1, possibly due to reduced lipid peroxidation, increased antioxidant systems, and inhibiting the apelin/TGF-ꞵ signaling pathway.

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Indication	Highest Phase	Country/Location	Organization	Date
Multiple Sclerosis	Preclinical	US	Q Therapeutics, Inc.	19 Sep 2024
Spinal Cord Injuries	Preclinical	US	Q Therapeutics, Inc.	19 Sep 2024
Stroke	Preclinical	US	Q Therapeutics, Inc.	19 Sep 2024
Amyotrophic Lateral Sclerosis	Discovery	JP	ReproCELL, Inc.	-
Amyotrophic Lateral Sclerosis	Discovery	JP	Q Therapeutics, Inc.	-
Transverse Myelitis	Discovery	JP	Q Therapeutics, Inc.	-
Transverse Myelitis	Discovery	JP	ReproCELL, Inc.	-

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