iNOS Polyclonal Antibody
- Known as:
- iNOS Polyclonal Antibody
- Catalog number:
- ASAKAS-NO001D
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- iNOS Polyclonal Antibody
Related genes to: iNOS Polyclonal Antibody
- Gene:
- NOS2 NIH gene
- Name:
- nitric oxide synthase 2
- Previous symbol:
- NOS2A
- Synonyms:
- iNOS, NOS, HEP-NOS
- Chromosome:
- 17q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-15
- Date modifiied:
- 2015-12-04
Related products to: iNOS Polyclonal Antibody
Related articles to: iNOS Polyclonal Antibody
- Inflammatory response and oxidative stress interact with each other and are involved in the pathogenesis of various chronic diseases. Senkyunolide A (SenA) is a phthalide compound isolated from the traditional Chinese medicine Chuanxiong Rhizoma (Ligusticum chuanxiong Hort.). At present, the anti‑inflammatory and anti‑oxidative stress effects of SenA remain unclear. In this study, we adopted an integrated strategy combining network pharmacology, bioinformatics analysis, molecular docking, molecular dynamics simulation, bio‑layer interferometry (BLI), and in vitro experiments to explore the anti‑inflammatory and anti‑oxidative stress effects and potential targets of SenA. Through network pharmacology and bioinformatics analysis, we identified four core target genes (Il1b, Ptgs2, Nos2, and Hmox1) of SenA against LPS‑induced inflammation in RAW264.7 cells. Direct binding of SenA to IL‑1β and PTGS2 was confirmed by molecular docking, molecular dynamics simulation, and BLI assays. In vitro experiments showed that SenA pretreatment effectively inhibited LPS‑induced inflammatory response and oxidative stress in RAW264.7 cells, as evidenced by reduced expression of pro‑inflammatory cytokines (TNF‑α, IL‑6, and IL‑1β), decreased levels of NO, ROS, and MDA, increased GSH levels, and alleviated cell swelling and mitochondrial damage. In addition, SenA pretreatment downregulated the mRNA expression levels of the core target genes Il1b, Ptgs2, Nos2, and Hmox1. In conclusion, our findings demonstrate that SenA exerts significant anti‑inflammatory and anti‑oxidative stress effects and may serve as a candidate compound for the treatment of inflammation‑related diseases. - Source: PubMed
Publication date: 2026/07/03
Liu YueYang GuangChi XiansuWang LiudingZhang YunfanLiang XiaoZhang Yunling - Genistein is a dietary isoflavone that is abundant in soy products and has been suggested to exert cardiovascular protective effects; however, its role in hypertension remains incompletely defined. Here, we investigated whether genistein ameliorates angiotensin II (Ang II)-induced hypertension and endothelial dysfunction using complementary , , and models. The oral administration of genistein substantially attenuated Ang II-induced elevations in systolic and diastolic blood pressure in mice without affecting body weight. Histological analyses revealed that genistein alleviated aortic wall thickening and smooth muscle hypertrophy, whereas vascular reactivity assays demonstrated improved endothelium-dependent relaxation while preserving the endothelium-independent responses. In isolated murine aortic rings, genistein reversed Ang II-induced hypercontractility and restored acetylcholine-mediated vasodilation. Furthermore, in human umbilical vein endothelial cells, genistein suppressed the Ang II-induced overproduction of reactive oxygen species (ROS) and restored nitric oxide (NO) bioavailability. Mechanistically, genistein improved endothelial redox-NO coupling, accompanied by transcriptional remodeling of the redox/NO axis [e.g., suppression of nicotinamide adenine dinucleotide phosphate oxidase 4 () and nitric oxide synthase 2 () and restoration of nitric oxide synthase 3 ()], which is consistent with reduced ROS and enhanced NO bioavailability. Collectively, our findings identify genistein as a potent endothelial-protective agent that ameliorates Ang II-induced hypertension, highlighting its therapeutic potential in cardiovascular disease driven by vascular dysfunction. - Source: PubMed
Publication date: 2026/06/16
Ku CunFeng HanxiaoWu ManniXie JiyuJiang KuanLi ChenhangQin ZichunAyan AbdrakhmanovZhang Yang - To explore the effects and mechanisms of broccoli-derived extracellular vesicles (BEVs) on wound healing of full-thickness skin defects in diabetic mice. This study was an experimental study using a group design and a repeated-measures design. BEVs were isolated and purified using ultrafiltration concentration combined with size-exclusion chromatography, and were successfully identified. According to the random number table method, mouse RAW264.7 cells were divided into a control group cultured under routine condition, as well as a lipopolysaccharide (LPS) group and a BEV group, in which cells were first stimulated with LPS for 12 hours and then respectively cultured under routine condition and with BEV. After 24 hours of culture, Western blotting was used to detect the protein expression levels of inducible nitric oxide synthase (iNOS) and arginase-1 (Arg-1) in cells. Immunofluorescence method was used to detect the protein expression levels of CD86 and CD206 in cells. The level of reactive oxygen species in cells was measured using the 2',7'-dichlorodihydrofluorescein diacetate fluorescence probe assay. The mRNA expression levels of nuclear factor-erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in cells were detected using the real-time fluorescence quantitative reverse transcription polymerase chain reaction method. The sample sizes for all of the above experiments were 3. Twenty-four 7-week-old male db/db mice were used, and a full-thickness skin defect wound was created in the dorsal region. The mice were then assigned to control group and BEV group according to the random number table method, with 12 mice in each group. At post injury day (PID) 0 (immediately), 3, 6, and 9, normal saline and 1×10 particles/mL BEVs solution were injected into the wound sites of mice in control group and BEV group, respectively. Wound healing was assessed at PID 0, 3, 6, 9, and 12, and wound healing rates were calculated at PID 3, 6, 9, and 12. At PID 6, the proportion of CD86- and CD206-positive areas in the wound tissue was assessed using the immunofluorescence method, and the level of reactive oxygen species in the wound tissue was measured using the dihydroethidium fluorescence probe assay. After 24 hours of culture, compared with those in control group, the protein expression levels of iNOS and CD86 of cells in LPS group were significantly elevated (<0.05), and the level of reactive oxygen species was significantly increased (<0.05). Compared with those in LPS group, the cells in BEV group showed significantly reduced protein expression levels of iNOS and CD86 (<0.05), significantly increased protein expression levels of Arg-1 and CD206 (<0.05), significantly decreased level of reactive oxygen species (<0.05), and significantly increased mRNA expression levels of Nrf2 and HO-1 (<0.05). From PID 0 to 12, wounds of mice in both control group and BEV group gradually healed. Specifically, at PID 3, 6, 9, and 12, the wound healing rates of mice in BEV group were significantly higher than those in control group (with values of 5.98, 5.79, 7.40, and 8.67, respectively, <0.05). At PID 6, the proportion of CD86-positive area in the wound tissue of mice in BEV group was (0.60±0.29)%, which was significantly lower than (1.61±0.19)% in control group (=7.20, <0.05); the proportion of CD206-positive area in the wound tissue of mice in BEV group was (3.42±0.77)%, which was significantly higher than (0.66±0.20)% in control group (=8.48, <0.05); the level of reactive oxygen species in the wound tissue of mice in BEV group was significantly lower than that in control group (=8.38, <0.05). BEVs can restore the "immuno-oxidative" homeostasis of full-thickness skin defect wounds in diabetic mice by activating the Nrf2/HO-1 axis, inducing the polarization of macrophages from the M1 phenotype to the M2 phenotype, and decreasing the level of reactive oxygen species, thereby significantly accelerating the wound healing process. - Source: PubMed
Shen QJian NZhang C PFu X B - Inflammatory diseases arise from complex interactions between immune signaling and cellular stress. Although endoplasmic reticulum (ER) stress is a key modulator of immunity, the mechanisms by which it promotes inflammatory pathology remain incompletely understood. Notably, ER stress-induced NF-κB activation alone is insufficient to account for robust IL-6 production, thus suggesting the involvement of additional regulators. Using bone marrow-derived macrophages and sepsis model mice, we identified the inducible transcription factor IκBζ as a critical mediator of this response, with ER stress synergizing with TLR signaling to markedly upregulate IκBζ. Mechanistically, ER stress triggered calcium-dependent signaling that led to IκB kinase-mediated degradation of the RNase Regnase-1, likely stabilizing Nfkbiz mRNA and promoting the accumulation of IκBζ, which was found to cooperate with the ER stress factor XBP1s to drive transcription of selected secondary-response genes, particularly Il6 and Nos2. Importantly, this synergy was required for excessive IL-6 production in septic mice, highlighting a gene-specific amplification pathway. Together, these findings identify a dual mechanism in which transcriptional synergy between IκBζ and XBP1s is coupled to posttranscriptional mRNA stabilization via Regnase-1 degradation, thereby linking proteotoxic stress to hyperinflammatory responses. Our results establish ER stress-mediated IκBζ accumulation as a key driver of inflammatory pathogenesis and a potential therapeutic target in ER stress-associated inflammatory disorders. - Source: PubMed
Nakaminami YuriRuengsinpinya LerdluckSakihara RikoTakahata YoshifumiHata KenjiIwawaki TakaoNishimura RikoMurakami Tomohiko - Plasticizers, including phthalate esters and phthalate-free alternatives, are widely detected environmental chemicals. Although increasing evidence suggests that plasticizers may disrupt gastrointestinal homeostasis, their potential molecular links with inflammatory gastrointestinal disorders (IGDs) remain unclear. - Source: PubMed
Publication date: 2026/06/07
Chen YongqiShi JiyuanRuan YunGuan JinghanYan MiaohanZhang ZongyingWu LuojinSang MengmengWang XinfengMao LimingLiu Zhaoxiu