Goat Interleukin 4,IL-4 ELISA Kit
- Known as:
- Goat Interleukin 4,Interleukin-4 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- kn0008go
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kono Biotech
- Gene target:
- Goat Interleukin 4 IL-4 ELISA Kit
Related genes to: Goat Interleukin 4,IL-4 ELISA Kit
- Gene:
- IL4 NIH gene
- Name:
- interleukin 4
- Previous symbol:
- -
- Synonyms:
- BSF1, IL-4, BCGF1, BCGF-1, MGC79402
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-10
- Date modifiied:
- 2016-10-05
- Gene:
- TLR2 NIH gene
- Name:
- toll like receptor 2
- Previous symbol:
- -
- Synonyms:
- TIL4, CD282
- Chromosome:
- 4q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-25
- Date modifiied:
- 2016-10-25
Related products to: Goat Interleukin 4,IL-4 ELISA Kit
Related articles to: Goat Interleukin 4,IL-4 ELISA Kit
- Allergic airway inflammation, a hallmark of asthma, is commonly driven by environmental allergens such as house dust mite (HDM). This study examined the protective effects of caraway (Carum carvi) and marjoram (Origanum majorana) extracts in a rat model of HDM-induced allergic airway inflammation. Daily HDM intranasal administration was applied over four weeks, with or without concurrent oral administration of the herbal extracts. Both treatments significantly reduced airway inflammation, total serum IgE, and pro-inflammatory cytokines (IL-6 and TNF-α), as well as the regulatory cytokine IL-10 in bronchoalveolar lavage fluid (BALF). RT-qPCR revealed a marked downregulation of Th2-associated cytokines (IL-4, IL-5, and IL-13) and the mucus-related gene Muc5ac, along with the restoration of the regulatory marker Foxp3. Consistently, ELISA analysis of BALF showed partial recovery of the Th1 cytokine IFN-γ. Western blotting confirmed reduced protein expression of NF-κB and STAT6 in treated groups. Histological examination showed notable improvement in lung architecture. Collectively, these findings suggest that caraway and marjoram attenuate HDM-induced airway inflammation through immunomodulatory and anti-inflammatory mechanisms, supporting their potential as complementary therapeutic agents for allergic asthma. - Source: PubMed
Publication date: 2026/04/20
Refaat Ahmed MMohammed Honyda SAli FaroukMohamed HebaAbdallah RaniaAbdel-Salam Bahaa K A - PARP14, a pivotal mono-ADP-ribosyltransferase, has been reported to promote the development of inflammatory diseases via IL-4/STAT6/Th2 and IL-6/STAT3/Th17 signaling axes, making it an attractive therapeutic target for related disorders. Herein, we employed structure-based virtual screening and subsequent structural optimization to identify a series of novel PARP14 inhibitors featuring a phthalazinone scaffold. Among them, compound exhibited strong PARP14 inhibitory activity (IC = 3.03 nM), exceptional selectivity, and robust suppression of PARP14-mediated mono-ADP-ribosylation (MARylation) in cell-based assays. In a dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD)-like mouse model, significantly attenuated skin lesions and effectively decreased the expression of key inflammatory factors, including IL-4, IL-13, IgE, and IL-17A, demonstrating superior efficacy compared with RBN-3143 and Upadacitinib. In short, our findings establish as a novel and potent PARP14 inhibitor with promising therapeutic potential against AD. - Source: PubMed
Publication date: 2026/04/20
Wu ShiqiCong KaiyuanLiu JingQu LeZeng XiaorongKong XiangyingLi ZiyueLou ShaoxueWei PingShao LiGu HongfengZhao YanXu QinlongChu ZhaoxingHe GuangweiZhu QihuaXu YungenZou Yi - Induced membrane technique (IMT), a novel approach for reconstructing critical-size bone defect, encounters the challenge of lengthy mineralization time after bone grafting. This study is to explore the effect of Naringin on M2 macrophage polarization-mediated osteogenesis in the induced membrane's bone graft area. - Source: PubMed
Publication date: 2026/04/15
Li ShuyuanYe JinfeiYang DawenCai QunbinZeng ZhanpengZhou Qishi - Histone deacetylase 6 (HDAC6), a member of the class IIb HDAC family, plays a crucial role in epigenetic regulation and cytoskeletal dynamics, while participating in host anti-infective immune responses. However, its precise functions and mechanisms during () infection remain incompletely defined. Our study demonstrated that respiratory infection upregulates HDAC6 expression at the infection site and in immune organs. Comparative analysis of wild-type (WT) and HDAC6-deficient (HDAC6) mice in this infection model revealed that HDAC6 deficiency exacerbates disease progression, including significant weight loss, severe pulmonary inflammation, and impaired clearance. Relative to WT mice, HDAC6 mice exhibited elevated Signal Transducer and Activator of Transcription 6 () and GATA Binding Protein 3 () mRNA expression, enhanced pathological Th2 responses with increased IL-4 secretion, and no significant differences in protective Th1 or Th17 responses following infection. Concurrently, these mice displayed enhanced M2 macrophage polarization, as evidenced by upregulated CD206 and Arg-1 expression, whereas M1 marker expression remained unchanged. The vitro studies confirmed that HDAC6 bone marrow-derived macrophages (BMDMs) promote M2 polarization, characterized by increased Arg-1, IL-10, and TGF-β production, and further co-culture experiments showed that -stimulated HDAC6 BMDMs drive Th2 differentiation. These findings elucidate the critical role of HDAC6 in regulating Th2-M2 immune responses during respiratory infection and suggest targeted modulation of HDAC6 as a novel therapeutic strategy for chlamydial respiratory infection. - Source: PubMed
Publication date: 2026/03/26
Yu JinxiYang ShuainiZha XiaoyuTuo YuqingSun RuoyuanZhang HongTan LuBai Hong - M2-like macrophages play a critical role in breast cancer progression. Although JMJD3 is reported to play a significant role in M2-like macrophage polarization, its precise mechanism remains unclear. By using PMA, IL-4, and IL-13, we successfully induced THP-1 cells into M2-like macrophages, which subsequently promoted breast cancer cell proliferation and inhibited apoptosis, accompanied by increased JMJD3 expression. We demonstrated that JMJD3 enhances M2-like macrophage polarization: knockdown of JMJD3 decreased the M2-like macrophage gene expression, while overexpression of JMJD3 produced the opposite effects. Furthermore, JMJD3 promoted M2-like macrophage polarization through the STAT6/IRF4 axis. Knockdown of JMJD3 abrogated IL-4/IL-13 induced IRF4 expression, while overexpression of JMJD3 upregulated IRF4 expression. Inhibition of STAT6 downregulated the expression of JMJD3, IRF4, and M2-like macrophage marker genes. Additionally, inhibiting JMJD3 and STAT6 in macrophages increased cell apoptosis and decreased cell viability in breast cancer cells, while JMJD3 overexpression exhibited pro-tumor activity. In conclusion, our findings highlight the role of JMJD3 in regulating M2-like macrophage polarization and its impact on breast cancer development through the STAT6/IRF4 axis. - Source: PubMed
Publication date: 2026/04/09
Lyu JuanWang EnqinLyu ShanmeiQian YingYe FenXu XiupingWang QingLu TaoHu LiangfengXu HongkunZhang Lihong