Proteins IL-6 , Human
- Known as:
- Proteins Interleukin-6 , Human
- Catalog number:
- C009
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins IL-6 Human
Related genes to: Proteins IL-6 , Human
- Gene:
- CEBPB NIH gene
- Name:
- CCAAT enhancer binding protein beta
- Previous symbol:
- TCF5
- Synonyms:
- LAP, CRP2, NFIL6, IL6DBP, C/EBP-beta
- Chromosome:
- 20q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1991-02-27
- Date modifiied:
- 2018-02-23
- Gene:
- CEBPD NIH gene
- Name:
- CCAAT enhancer binding protein delta
- Previous symbol:
- -
- Synonyms:
- CRP3, CELF, C/EBP-delta, NF-IL6-beta
- Chromosome:
- 8q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-24
- Date modifiied:
- 2018-02-23
- Gene:
- ENTPD6 NIH gene
- Name:
- ectonucleoside triphosphate diphosphohydrolase 6
- Previous symbol:
- CD39L2, IL6ST2
- Synonyms:
- NTPDase-6, dJ738P15.3
- Chromosome:
- 20p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-20
- Date modifiied:
- 2019-02-28
- Gene:
- IL6 NIH gene
- Name:
- interleukin 6
- Previous symbol:
- IFNB2
- Synonyms:
- IL-6, BSF2, HGF, HSF
- Chromosome:
- 7p15.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2017-07-12
- Gene:
- IL6RP1 NIH gene
- Name:
- interleukin 6 receptor pseudogene 1
- Previous symbol:
- IL6RL1
- Synonyms:
- -
- Chromosome:
- 9q22.2
- Locus Type:
- pseudogene
- Date approved:
- 1991-08-18
- Date modifiied:
- 2014-11-19
Related products to: Proteins IL-6 , Human
Related articles to: Proteins IL-6 , Human
- This study aimed to examine the associations between trimester-specific bisphenol exposure and preterm birth (PTB) and explore potential underlying mechanisms. - Source: PubMed
Publication date: 2026/05/14
Lv DanChen ShiyaoLuo YaoyuLi XufangPraseth LeakanaHan JiaqiXian JunrongLi FanfanHe MengzhouFan YaoXu HezeZhou QiongLi WeiLiu LiLin XingguangShen XiantaoYe FangDeng Dongrui - Agaricus bisporus contains bioactive proteins, including tyrosinase, which may influence dopaminergic metabolism. Parkinson's disease (PD) is characterized by degeneration of dopaminergic neurons driven by oxidative stress, neuroinflammation, and apoptosis. - Source: PubMed
Publication date: 2026/05/14
Zhgenti NikolozBibilashvili OtarDavitashvili EleneKoshoridze Nana - Diabetic nephropathy is an early complication of diabetes, which triggers lipotoxicity, oxidative stress, inflammation, fibrosis, and apoptosis. This study aimed to investigate the possible protective effects of Cafestol and the underlying molecular mechanisms in type 1 diabetes-induced nephropathy. One dose of streptozotocin (65 mg/kg, i.p.) was used to induce diabetes, then Cafestol was given orally at 5 and 10 mg/kg for eight weeks. In the control rats, Cafestol (10 mg/kg) did not cause any significant changes to any of the measured parameters, including 24-hour urine volume, urinary albumin, creatinine, and renal injury parameters (KIM-1, NGAL, nephrin), suggesting that Cafestol has no adverse renal effect in normal physiology. In T1DM induction rats, renal dysfunction was apparent as marked increases in urine output, enzymatic indicators of injury, inflammatory mediators (IL-6, TNF-α, ICAM-1, nuclear NF-κB), oxidative stress (MDA), and glycation markers (AGEs, sRAGEs), while there were significant decreases in antioxidant defenses (HO-1, SOD, GSH) and nuclear Nrf2 expression. Treatment with Cafestol at doses of 5 mg/kg and 10 mg/kg significantly reduced the pathological parameters when compared to T1DM alone in a dose-dependent manner. Cafestol treatment reduced glomerular and tubular injury, inhibited renal inflammation, restored oxidative balance, and improved antioxidant capacity. Cafestol treatment also reduced renal Keap1 mRNA expression and increased cytoplasmic and nuclear Nrf2 protein levels, indicating that Cafestol activates the Nrf2 pathway without altering Nrf2 mRNA expression. Further, co-administration of Brusatol, an Nrf2 inhibitor, eliminated the renal protection effects of Cafestol for all measured parameters and returned levels to T1DM alone. The results suggest that Cafestol provides substantial renal protective, anti-inflammatory, and antioxidative benefits in a model of diabetes, mainly through the activation of Nrf2. This finding suggests that Cafestol may be a novel agent to activate Nrf2, which may have implications for the treatment of DN. - Source: PubMed
Publication date: 2026/05/14
Sinan Nujud AAlmujaydil Mona S - Helicobacter pylori (H. pylori) is a highly pathogenic microorganism that can cause various gastric diseases. Accumulating evidences have demonstrated probiotics' potential in combating H. pylori infections. The aim of this study was to explore the effects and underlying mechanism of Lactobacillus casei (L. casei) HY001 against the gastric inflammation and gastric microbiota alteration induced by H. pylori infection. These results indicated that L. casei HY001 significantly inhibited the growth of H. pylori SS1, decreased urease activity, and exhibited strong co-aggregation properties with H. pylori SS1 in vitro experiments. Furthermore, L. casei HY001 was found to be capable of inhibiting the adhesion of H. pylori SS1 with AGS cells. Subsequently, Experiments in animals suggested L. casei HY001 alleviated gastric inflammation by inhibiting the expression of NF-κ B and reducing pro-inflammatory mediator levels (IL-8, TNF-α, IL-1β, and IL-6). Moreover, the gastric microbiota 16S rRNA gene sequencing analysis revealed that L. casei HY001 improved the structure of the gastric microbiota by modulating the abundance of Firmicutes, Bacteroidota and Proteobacteria. Meanwhile, the relative abundances of Rothia, Clostridium-sensu-stricto-1, Alistipe and Prevotellacea-UG-001 were significantly increased. In contrast, the abundances of Helicobacter, Turicibacter, unclassified - Muribaculaceae, unclassified- Oscillospiraceae and Lachnospiraceae -NK4A136-group were significantly reduced following HY001 intervention. These researches indicated that L. casei HY001 improved H. pylori SS1 induced gastric mucosal damage in mice, regulated immune factors, enhanced the reduced diversity of gastric Lachnospiraceae microbiota caused by H. pylori infection, and restored the stability of the microbial community structure. - Source: PubMed
Publication date: 2026/05/14
Lv ZhonghuaYu JunqingZhang XuetingZhang LeiZhang ChunleiLiu XiaoxuChang YuYin HangWang WeiZhao HaidanLi Huicheng - Acute gouty arthritis (AGA) is a common inflammatory joint disease characterized by pain resulting from the deposition of monosodium urate (MSU) crystals into joints and surrounding tissues. RGFP966, a selective inhibitor of histone deacetylases 3 (HDAC3), can down-regulate the AIM2 inflammasomes. This study aimed to explore the mechanism of action of RGFP966 in MSU-induced AGA. MSU-induced AGA rats were treated with RGFP966 or colchicine, and physiological and pathological indicators were determined. The rat joint synovial tissues and kidneys pathological damage was observed by hematoxylin and eosin staining. Enzyme-linked immunosorbent assay (ELISA), Western blot, JC-1 staining, mitochondrial membrane potential (MMP) measurement, ATP assay, and immunofluorescence were applied to evaluate the effects of RGFP966 on the AIM2 inflammasomes and mitophagy. In MSU-induced AGA rats, RGFP966 significantly improved the gait score, the swelling degree and synovitis score. In addition, RGFP966 repressed the increased serum levels of IL-1β, IL-18, IL-6 and TNF-α, and reduced the protein levels of AIM2, Pro-caspase-1, Cleaved-caspase-1, ASC, Pro-IL-1β, and Cleaved-IL-1β in MSU-induced AGA rats. Furthermore, RGFP966 decreased the level of reactive oxygen species (ROS), increased the level of ATP and MMP, and promoted the levels of Pink1, Parkin and LC3-II. Collectively, RGFP966 significantly alleviated AGA, and the underlying mechanism is related to promote mitophagy by inhibiting the activation of the AIM2 inflammasomes. - Source: PubMed
Publication date: 2026/05/14
Wang ZeweiLiu ChunyangCheng FengShi XiuyunDai JingTian JingJin HongxuLiu Ying