GSTA3 Mouse Monoclonal Antibody
- Known as:
- GSTA3 Mouse Monoclonal Antibody
- Catalog number:
- BIN-002940-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- GSTA3 Mouse Monoclonal Antibody
Related genes to: GSTA3 Mouse Monoclonal Antibody
- Gene:
- GSTA3 NIH gene
- Name:
- glutathione S-transferase alpha 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 6p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-04-29
- Date modifiied:
- 2015-09-10
Related products to: GSTA3 Mouse Monoclonal Antibody
Related articles to: GSTA3 Mouse Monoclonal Antibody
- Heat stress (HS) causes organ damage and has detrimental impacts on the welfare and production in broilers. As a crucial immune organ, the spleen exerts a key role in immune homeostasis of broilers. Fucoidan (FUC) is a marine functional substance and extracted from seaweeds with multiple biological activities, such as anti-inflammatory and antioxidant effects. This experiment attempted to investigate the protective effect of fucoidan on HS-induced spleen injury in broilers. A total of 240 male Arbor Acres (AA) broilers at 21 d of age were randomly assigned to five groups: control (CON) group, HS group, and HS group supplemented with 200 (HS+FUC), 400 (HS+FUC) and 800 (HS+FUC) mg/kg FUC. The feeding trial lasted 21 d. The results showed that HS reduced the spleen index, impaired antioxidant capacity, and induced pathological damage in the spleens of broilers. Dietary supplementation with 200, 400, and 800 mg/kg FUC alleviated these injuries. Specifically, 800 mg/kg FUC improved the spleen index, antioxidant indicators and the splenic histomorphological pathology in broilers under HS. Therefore, 800 mg/kg of FUC was identified as the effective dosage for mitigating HS-induced splenic injury in broilers. Accordingly, this study further investigated the molecular mechanism of the beneficial effects of 800 mg/kg FUC. FUC upregulated the expression of antioxidant genes (NQO1, CAT, SOD1, SOD2, GCLC, GCLM, GSTA3, HO-1) and ferroptosis-related genes (GPX4, SLC7A11, Fpn1, FTH1), while downregulating the expression of inflammatory genes (IL-1β, IL-4, TNF-α, NF-κB) in the spleen of heat-stressed broilers. Besides, FUC reduced the protein expression of total P65 and p-P65, and enhanced the protein expression of total Nrf2 and p-Nrf2 in the spleen of heat-stressed broilers. The findings demonstrated that dietary supplementation of 800 mg/kg FUC alleviates HS-induced spleen damage in broilers by reducing the oxidative stress, ferroptosis and inflammation, and the protective role of FUC is related to the activation of Nrf2 signaling and the suppression of NF-κB signaling. This study offers theoretical support for applying FUC in improving the spleen health of broilers under HS conditions. - Source: PubMed
Publication date: 2026/04/27
Liu Qian-QianChen YueLiang Qi-HaoTian Shan-ZiYao Qing-HuaYe Xue-QingChen Jun-HongLiu Wen-Chao - Heat stress (HS) is a significant challenge in broilers, which has a negative impact on liver health and metabolic function, endangering broiler production. This study aimed to evaluate the protective effects of dietary fucoidan (FUC) in mitigating HS-induced liver injury and to elucidate the underlying mechanisms. A total of 240 male Arbor Acres (AA) broilers at 21 days of age were randomly divided into five groups: thermoneutral (TN) group, HS group, and HS group supplemented with 200, 400, or 800 mg/kg FUC, respectively. Based on comprehensive assessments of liver histopathology, liver index, and serum biochemical markers-related to liver function (TP, ALB, AST, ALT), 800 mg/kg FUC was identified as the effective dose for alleviating HS-induced hepatic injury, resulting in improvements in liver architecture and function. Further investigations revealed that 800 mg/kg FUC enhanced hepatic antioxidant capacity by increasing T-AOC, T-SOD, and GSH-Px activities in broilers under HS. The non-targeted metabolomics analysis suggested that FUC improves six metabolites in the liver of broilers subjected to HS, including Glu-Asp-Gln, Asn-Pro-Tyr, Glu-Thr-Ile, N-Acetylleucylalanylserine, Octadecyl Fumarate, and Oleoyl-l-Carnitine. The differential metabolites were significantly enriched in several metabolic pathways, such as glycerophospholipid metabolism, fatty acid degradation, and ferroptosis. Furthermore, dietary FUC enhanced the expression of antioxidant genes (GCLC, GCLM, HO-1, SOD2, GPX1, GPX3, CAT1, and GSTA3), suppressed lipogenic genes (SREBP-1, FAS, and ACC), and upregulated the lipolytic gene ATGL as well as the adipogenic regulator PPARγ in the liver of broilers under HS. Additionally, FUC downregulated pro-ferroptotic genes (ACSL4, LPCAT3, and PTGS2) while upregulated anti-ferroptotic genes (Fpn1, FTH1 and SLC7A11) in the liver of heat-stressed broilers. Western blot analysis confirmed that FUC activated the Nrf2 signaling pathway by increasing the protein expression of Nrf2, phosphorylated Nrf2 (p-Nrf2), and nuclear p-Nrf2, while upregulated the AMPK pathway by increasing AMPK and phosphorylated AMPK (p-AMPK) protein levels of the liver in broilers subjected to HS. These findings indicate that dietary supplementation with 800 mg/kg FUC ameliorates HS-induced liver injury through the activation of Nrf2-mediated antioxidant and anti-ferroptosis signaling, and the regulation of AMPK-mediated lipid metabolism balance. This study provides a dietary strategy to improve liver health in heat-stressed broilers, which is beneficial for broiler production during the hot season. - Source: PubMed
Publication date: 2026/01/20
Liang Qi-HaoLiu Qian-QianTian Shan-ZiYao Qing-HuaYe Xue-QingLiu Wen-Chao - Uterine diseases in dairy cattle are associated with reduced fertility, but the specific mechanisms of disease-mediated subfertility are not known. We hypothesized that intrauterine infusion of Escherichia coli and Trueperella pyogenes would alter the endometrial transcriptome and compromise oocyte developmental competence after disease resolution. Non-lactating Holstein cows received an intrauterine infusion of either sterile phosphate-buffered saline (n = 29) or pathogenic E. coli and T. pyogenes (n = 32) on day 3 of the estrous cycle to induce acute endometrial inflammation. Oocytes of antral follicles were collected by ovum pick-up following estrous synchronization 23 days after intrauterine infusion and underwent in vitro embryo production. Endometrial samples were collected on day 16 of the estrous cycle via cytobrush 41 days after infusion and analyzed by RNA sequencing. Bacterial infusion had no effect on oocyte development to the blastocyst stage, but increased blastocyst expression of CDK7, CHSY1, and LSM4 and tended to reduce the molecular signature of embryo competence for survival. Bacterial infusion altered the expression of 203 genes in the endometrium 41 days after infusion, increasing expression of GSTA3, PVALB, JAKMIP2, FOLH1B, and TCF23, and decreasing expression of MYMK, LOC104974498, CDRT1, KIAA0408, and SLC45A2. Differentially expressed genes were annotated to 54 canonical pathways, with glutathione-mediated detoxification being the top predicted pathway activated following bacterial infusion. Collectively, this work demonstrates that bacterial infections can have lasting effects on the uterus and potentially reduce the molecular competence of oocytes, providing a link to the long-term subfertility of cows after uterine disease. - Source: PubMed
Seekford Zachary KTariq ArslanHaimon McKenzie L JHoorn Quinn AMacay Gabriela AZhai YutingBlock JeremyRabaglino Maria BelenJeong Kwangcheol CHansen Peter JBromfield John J - Ovarian aging is considered the "pacemaker" and "biological clock" of systemic female aging, with early manifestations that are often insidious. In this study, we analyzed the shared and distinct molecular signatures between physiological and pathological ovarian aging models using proteomic approaches, with the aim of identifying early predictive markers and therapeutic targets for ovarian aging, evaluating model fidelity, and elucidating underlying molecular mechanisms. - Source: PubMed
Publication date: 2025/11/28
Bai MengyingZhang LiujuanWu WenboWeng RuoxinWu HaifengLi YuanLing ShuyiZheng Yuehui - Dioxins are highly toxic and persistent environmental pollutants. The liver, with its complex enzymatic system, plays a crucial role in their detoxification. Hepatic lipid droplets (LDs) are specialized organelles with diverse biological functions, yet their role in dioxin toxicity remains poorly understood. This study investigates the impact of TCDD, the most potent dioxin congener, on the biochemical properties and functionality of hepatic LDs in exposed mice. Female and male BALB/c mice (12-14 weeks old) received a single oral dose of 15-25 µg/kg bw, designated as TCDD-F, TCDD-M, TCDD-F, and TCDD-M. TCDD exposure induced a dose-dependent increase in liver weight, suggesting hepatomegaly. The number of hepatic LDs and their protein composition increased, with greater hydroxylation enzymatic activity observed in males. HPLC analysis confirmed that hepatic LDs in both sexes accumulated and stored TCDD, raising concerns about potential long-term effects. Moreover, gene expression analysis revealed significant alterations in hepatotoxicity markers (Ahr, Arnt, Cyp1a1, Gsta1, Gsta3), oxylipin biosynthesis genes (Lox15, Cox2), and LD formation genes (Plin5, Cidec, Ppara, Pparg) in a dose-, time-, and sex-dependent manner. These findings offer insight into how lipophilic pollutants are sequestered and metabolized, aiding strategies to reduce dioxin toxicity and treat related liver disorders. - Source: PubMed
Publication date: 2025/11/19
Hammoudeh NourSoukkarieh ChadiHanano Abdulsamie