2. Immunology/Inflammation Autophagy PI3K/Akt/mTOR Stem Cell/Wnt MAPK/ERK Pathway
  3. Complement System Autophagy mTOR Akt PI3K ERK Interleukin Related
  4. Lipoteichoic acid

Lipoteichoic acid  (Synonyms: 脂磷壁酸)

目录号: HY-N9481
COA 产品使用指南

摩尔计算器

Lipoteichoic acid 是口服有效的抗炎剂和抗肿瘤剂。Lipoteichoic acid 是革兰氏阳性菌中重要的免疫分子，可通过诱导 C3 和抑制 CD55 来激活补体系统。Lipoteichoic acid 通过 PI3K/Akt/mTOR 通路调控巨噬细胞自噬 (autophagy)。Lipoteichoic acid 在小鼠中可诱导肺损伤。Lipoteichoic acid 可抑制黑色素的产生。

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Lipoteichoic acid Chemical Structure

Lipoteichoic acid Chemical Structure

CAS No. : 56411-57-5

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Lipoteichoic acid 相关抗体

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  • 生物活性

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  • 参考文献

生物活性

Lipoteichoic acid is an orally effect anti-inflammatory and antitumor agent. Lipoteichoic acid is a crucial immune molecule in Gram-positive bacteria that activates the complement system by inducing C3 and inhibiting CD55. Lipoteichoic acid regulates macrophage autophagy through the PI3K/Akt/mTOR pathway. Lipoteichoic acid induces lung damage in mice. Lipoteichoic acid inhibits the production of melanin[1][2][3][4][5][6][7].

体外研究
(In Vitro)

Lipoteichoic acid (0.1-20 μg/mL；12-48 小时) 通过抑制 PI3K/AKT/mTOR 通路诱导巨噬细胞自噬[2]。
Lipoteichoic acid (0.1-100 μg/mL；24 小时) 在 B16F10 细胞中通过 MITF、 ERK 和 PI3K/AKT 信号通路抑制黑色素的产生[3]。
Lipoteichoic acid (50-100 ng/mL；2-3 小时) 对 HT-29 细胞无细胞毒性，在 LPS (HY-D1056) 处理的 HT-29 细胞中降低 TNF-α 的分泌和提高 IL-10 的分泌[4]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Lipoteichoic acid 相关抗体:

Western Blot Analysis[2]

Cell Line: macrophage
Concentration: 0.1, 1, 10, and 20 μg/mL
Incubation Time: 12, 24 and 48 h
Result: Significantly decreased the expression levels of p-Akt and p-mTOR protein, but did not affect the expression of Akt and mTOR protein.

Western Blot Analysis[3]

Cell Line: B16F10 cells
Concentration: 0.1, 1, 10 and 100 μg/mL
Incubation Time: 24 h
Result: Reduced the level of MITF in a dose-dependent manner.
Increased the phosphorylation levels of ERK, AKT and PI3K.
体内研究
(In Vivo)

Lipoteichoic acid (800 μg/100 μL；灌胃；7 天) 在结肠炎小鼠模型中具有改善作用[4]。
Lipoteichoic acid (0.1 mg；口服；20 天-34 周) 在 UV 诱导的肿瘤模型中具有免疫调节和保护作用[5]。
Lipoteichoic acid (5 mg/kg；气管内注射；单剂量) 在小鼠中可诱导肺损伤[6]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: DSS (HY-116282C) treated male swiss albino mice aged 6-8 weeks old[4]
Dosage: 800 μg/100 μL
Administration: Oral gavage (i.g.); 7 days
Result: Significantly improved external colitis symptoms, disease activity scores, and weight gain in colitis mice.
Significantly improved key inflammatory markers such as the gut permeability, myeloperoxidase activity and histopathological damages in colon in colitis mice.
Animal Model: Female Crl:SKH-1-hrBR hairless mice aged 8-12 weeks old (20-25 g) with UV-induced tumors[5]
Dosage: 100 μL (1 mg/mL)
Administration: Oral administration; 20 days and 34 weeks (3 times a week)
Result: Caused T cells in the mouse inguinal lymph nodes to produce higher levels of interferon-γ and a number of total, helper and cytotoxic T cells.
Significantly delayed the appearance of tumors.
Animal Model: Male C57BL/6 mice aged 6‑8 weeks old (22±3 g)[6]
Dosage: 5 mg/kg
Administration: Intratracheal injection; Single dose
Result: Induced inflammatory cell infiltration, inter‑alveolar septal thickening and alveolar collapse.
Promoted the concentration of BALF total protein and the expression of inflammatory factors.
Increased lung neutrophil infiltration and MPO activity.
CAS 号
性状

固体

颜色

White to off-white

中文名称

脂磷壁酸；脂壁酸
结构分类
初始来源

Staphylococcus aureus
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

纯度 & 产品资料

COA (255 KB)

产品使用指南 (1538 KB)
参考文献

Lipoteichoic acid 相关分类

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Keywords:

Lipoteichoic acid56411-57-5脂磷壁酸脂壁酸Complement SystemAutophagymTORAktPI3KERKInterleukin RelatedMammalian target of RapamycinPKBProtein kinase BPhosphoinositide 3-kinaseExtracellular signal regulated kinasesILB16F10 cellsmacrophageHT-29 cellscomplement systemlung injury modelInhibitorinhibitorinhibit

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