Ask about this productRelated genes to: MYD88 Blocking Peptide
- Gene:
- MYD88 NIH gene
- Name:
- MYD88 innate immune signal transduction adaptor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-23
- Date modifiied:
- 2019-04-23
Related products to: MYD88 Blocking Peptide
Related articles to: MYD88 Blocking Peptide
- Sepsis-induced acute lung injury (ALI) poses a significant therapeutic challenge due to the lack of effective treatments. Shionone (SHI), a compound known for its anti-inflammatory properties, was investigated for its potential to mitigate ALI by modulating macrophage polarization, a key process in the inflammatory response. The underlying mechanism was also explored. - Source: PubMed
Wu QianXi GeyingLin YingZhao JunkaiSong YiJiang HuojunZhang Biao - Inflammation is an important pathological process in ischemic stroke (IS). Astaxanthin (ATX) is a natural product with neuroprotection effects. However, the mechanism of ATX on anti-inflammatory after IS is not clear. The aim of this study was to investigate the mechanism of ATX on anti-inflammatory after IS. Male Sprague-Dawley rats were used to establish a model of middle cerebral artery occlusion (MCAO) on one side and were pre-treated with gavage of ATX for 7 days. One day after MCAO, behavioral tests were conducted on the rats, and the brain tissues were subsequently collected. Transcriptomic sequencing (differentially expressed genes with fold change > 1 or < - 1 and FDR P value < 0.05 were selected), flow cytometry, brain water content, Western blot, HE staining, immunohistochemistry and ELISA were analyzed to evaluate the brain damage. ATX treatment has improved the neurological deficits and reduced brain edema, cerebral infarction volume, the expression of tight junction protein occludin, and apoptosis. Also, ATX has reduced inflammation and apoptosis-related proteins such as TLR4, MyD88, NFκB, IL-1β, IL-6, Cyt C, and Caspase-3. The protective effect of ATX was inhibited by the TLR4 agonist RS 09. ATX can improve nerve damage after IS, and these protective effects were realized by anti-inflammatory and anti-apoptosis. ATX alleviates apoptosis and inflammation of IS by inhibiting the TLR4 pathway. - Source: PubMed
Publication date: 2026/04/28
Gao ShanLi JinjianZhao YuetongWei ZhenRong ChunshuZuo KuiyangWang XuZhao Dexi - Docetaxel (DTX) is an efficient and normally used anticancer drug. But it results in systemic organ toxicity and damages various non-target organs of the body. Vanillic acid (VA) is a biologically active phenolic acid that exhibits potential therapeutic properties. This research was conducted to understand the protective effects of VA against DTX-induced liver damage in rats. Forty male Sprague Dawley rats were randomly assorted into four groups. One group was the control, and the other groups were as follows: DTX group, DTX + VA group, and VA group. Thirty milligrams per kilogram DTX was given once on the first day of the trial while VA (50 mg/kg) was given on a daily basis via intragastric gavage for 7 days. The results showed that DTX disrupted TLR4/MyD88/TRAF6, NF-κB, and JAK/STAT signaling pathways and caused oxidative stress, inflammation, and apoptosis as well as mitochondrial and histological damages in liver. However, the supplementation of VA protected the hepatic tissues from these damages by mitigating the effects of DTX. VA protected the hepatic tissues by reducing the expressions of TLR4, MyD88, TRAF6, NF-κB, and other inflammatory cytokines, while upregulating the expressions of IκB. Importantly, it lowered the levels of ALT and AST by 29.10% and 44.46%, respectively, while significantly reducing the levels of inflammatory markers, i.e., TNF-α (36.60%) and IL-6 (40.94%). Additionally, ELISA evaluation showed it lowered the levels of p-STAT3, and NF-κB (p-65) and normalized BAX, BCL-2 and CASPASE-3 expressions and levels. Furthermore, VA restored antioxidant defenses and preserved mitochondrial and histological architecture. Hence, VA may protect hepatic tissues from chemotherapeutic drug, i.e., DTX-induced damage through modulating JAK/STAT, and NF-κB/TLR4 signaling pathways. - Source: PubMed
Publication date: 2026/04/28
Maqsood ZainabGillani SumbalAkram ZarafshanHira HasoobaMinal Javed Khadija - Luteal phase defect (LPD) is a prevalent endocrine disorder contributing significantly to female infertility and early pregnancy loss. Nuangong Tiaojing Formula (NTF), a traditional Chinese medicine formula, has demonstrated clinical efficacy in treating LPD, yet its underlying mechanisms remain incompletely elucidated. - Source: PubMed
Publication date: 2026/04/17
Hao MingqianXue XiLi YinjiaWu XingchengGao YaqinCui YutingLi YunshuZhang MingtaoQin FeiLyu GaohongXu LiuZhou HuifangChen Zhipeng - Inflammation is closely linked to depression, and natural compounds show promise for treating inflammatory depression, though their mechanisms remain unclear. Eleutheroside B (EB), a key bioactive component of the classic Araliaceae plant Eleutherococcus senticosus with various central protective effects, but its antidepressant properties remain to be explored. - Source: PubMed
Publication date: 2026/04/26
Wu ShuoJiang YunhaoZhai CaiyuLi PeipeiYang HongyangXu ChiWang YujunLiu Jing-GenZhang Lesha