tlr 3

Polyinosinic-polycytidylic acid (Poly(I:C)) 是一种双链 RNA (dsRNA)，是一种 TLR3 激动剂。Polyinosinic-polycytidylic acid 可以诱导哺乳动物天然免疫。

TLR3-IN-1 (CU CPT 4a) 是一种选择性的TLR3信号抑制剂，在 RAW 264.7 细胞中 IC50 为 3.44 μM。它可以抑制 TLR3 dsRNA 复合物介导的下游信号通路，并抑制全细胞中 TNF-α 和 IL-1β 的产生。

Polyinosinic-polycytidylic acid sodium (Poly(I:C) sodium) 是双链 RNA 的合成类似物，是TLR3和视黄酸诱导型基因 I 受体激动剂。它可以用作疫苗佐剂，直接触发癌细胞发生凋亡，还增强先天性和适应性免疫反应，并改变肿瘤的微环境。

TLR7 8 agonist 3 是TLR7 8激动剂。

CU-CPT17e 是多Toll 样受体激动剂，可激活TLR3、TLR8和TLR9。

TLR7 agonist 3 是一种 Toll 样受体 7 (TLR7) 激动剂，具有抗癌活性，可用于研究免疫系统疾病。

Tri(TLR4-IN-C34-C2-amide-PEG1)-amide-C3-COOH为包括TLR4抑制剂TLR4-IN-C34的连接子。该化合物通过抑制肠细胞与巨噬细胞内TLR4活性，能够减轻内毒素血症及坏死性小肠结肠炎小鼠模型中的全身性炎症。

Tri(TLR4-IN-C34-C2-amide-C3-amide-PEG1)-amide-C3-COOH 是一种融合了TLR4-IN-C34抑制剂的连接子。这种抑制剂在阻断肠细胞与巨噬细胞内的TLR4上发挥作用，有效减轻了内毒素血症及坏死性小肠结肠炎小鼠模型中的全身性炎症现象。

Tri(TLR4-IN-C34-PEG2-amide-PEG1)-amide-C3-COOH 是一种含有 TLR4抑制剂 TLR4-IN-C34 的连接子。TLR4-IN-C34 抑制肠细胞和巨噬细胞中的TLR4，减少内毒素血症和坏死性小肠结肠炎小鼠模型的全身炎症。

Polygalasaponin F 是从瓜子金中提取的齐墩果烷型三萜皂苷，可通过调节TLR4-PI3K AKT-NF-kB 信号通路减少神经炎症细胞因子的分泌，能降低炎性细胞因子肿瘤坏死因子 α 的释放。

Givinostat (ITF-2357) is a HDAC inhibitor with an IC50 of 198 and 157 nM for HDAC1 and HDAC3, respectively. Givinostat (ITF2357) suppresses total LPS-induced IL-1β production robustly compared with the reduction by ITF3056. At 25, 50, and 100 nM, Givinostat reduced IL-1β secretion more than 70%. Givinostat (ITF-2357) suppresses the production of IL-6 in PBMCs stimulated with TLR agonists as well as the combination of IL-12 plus IL-18. IL-6 secretion decreases to 50% at 50 nM Givinostat, but at 100 and 200 nM, there is no reduction[1]. As shown by the CCK-8 assay, Givinostat (ITF-2357) inhibits JS-1 cell proliferation in a concentration-dependent manner. Treatment with Givinostat ≥500 nM is associated with significant inhibition of JS-1 cell proliferation (P<0.01). Also, the cell inhibition rate significantly differs between the group cotreated with Givinostat ≥250 nM plus LPS and the group without LPS treatment (same Givinostat concentration) (P<0.05)[2]. Givinostat (ITF2357) at 10 mg kg is used as a positive control and, as expected, reduced serum TNFα by 60%. Strikingly, pretreatment of ITF3056 starting at 0.1 mg kg significantly reduces the circulating TNFα by nearly 90%. To achieve a significant increase in serum IL-1β production, a higher dose of LPS is injected (10 mg kg), and blood is collected after 4 h. Similarly, when pretreated with lower doses of Givinostat (ITF-2357) (1 or 5 mg kg), there is a 22% reduction for 1 mg kg and 40% for 5 mg kg[1]. [1]. Li S, et al. Specific inhibition of histone deacetylase 8 reduces gene expression and production of proinflammatory cytokines in vitro and in vivo. J Biol Chem. 2015 Jan 23;290(4):2368-78. [2]. Wang YG, et al. Givinostat inhibition of hepatic stellate cell proliferation and protein acetylation. World J Gastroenterol. 2015 Jul 21;21(27):8326-39. [3]. Leoni F, et al. The histone deacetylase inhibitor ITF2357 reduces production of pro-inflammatory cytokines in vitro and systemic inflammation in vivo. Mol Med. 2005 Jan-Dec;11(1-12):1-15.

Ginsenoside Rg5 是红参的主要成分，可阻断IGF-1与其受体的结合，IC50约为90 nM。它还通过抑制NF-κB p65的 DNA 结合活性来抑制COX-2的 mRNA 表达。它可促进血管生成和改善高血压，具有抗炎和治疗阿尔茨海默病的潜力。

Sophocarpine 是一种从传统草药苦参中提取的重要生物碱。苦参具有抗病毒、抗肿瘤和抗炎等多种药理作用。它通过多种机制显著抑制癌细胞的生长，具有抗肿瘤活性。