2. Immunology/Inflammation NF-κB Cytoskeleton
  3. Toll-like Receptor (TLR) NF-κB Collagen Interleukin Related Cadherin NOD-like Receptor (NLR)
  4. Ligusticum cycloprolactam

Ligusticum cycloprolactam 是一种强效的具有口服活性的 TLR4/NF-κB 抑制剂，具有抗炎活性。Ligusticum cycloprolactam 可通过在体内外抑制 TLR4/NF-κB 信号通路来减轻肾损伤。Ligusticum cycloprolactam 可通过降低血清尿酸水平、减轻肾小管损伤、炎性浸润及间质胶原蛋白 (collagen) 沉积，缓解小鼠高尿酸血症肾病 (HN)，进而改善肾功能。Ligusticum cycloprolactam 可用于 HN 的相关研究。

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Ligusticum cycloprolactam

Ligusticum cycloprolactam Chemical Structure

CAS No. : 2283387-37-9

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Ligusticum cycloprolactam 相关抗体

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NLRP3 NLRP1 NOD1 NOD2

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Ligusticum cycloprolactam is a potent and orally active TLR4/NF-κB inhibitor, exhibiting anti-inflammatory activity. Ligusticum cycloprolactam alleviates renal injury by inhibiting the TLR4/NF-κB signaling pathway both in vivo and in vitro. Ligusticum cycloprolactam attenuates hyperuricemic nephropathy (HN) in mice by reducing serum uric acid, tubular damage, inflammatory infiltration, and interstitial collagen deposition, thereby improving renal function. Ligusticum cycloprolactam can be used for the research of HN[1].

IC50 & Target[1]

TLR4

 

IL-6

 

IL-1b

 

IL-1β

 

E-cadherin

 

NLRP3

 

体外研究
(In Vitro)

Ligusticum cycloprolactam (20-80 μM；作用 36 h) 可通过抑制 TLR4/NF-κB 信号通路、减轻炎症及纤维化反应，改善由 Uric acid (HY-B2130) 诱导的 NRK-52E 细胞损伤[1]。

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

Ligusticum cycloprolactam 相关抗体:

Western Blot Analysis[1]

Cell Line: NRK-52E cells
Concentration: 20, 40, 80 μM
Incubation Time: 36 h
Result: Decreased the levels of KIM-1, NLRP3, IL-1β, VCAM1, FN and α-SMA proteins, while enhancing E-cadherin protein expression, in a dose-dependent manner.

Real Time qPCR[1]

Cell Line: NRK-52E cells
Concentration: 20, 40, 80 μM
Incubation Time: 36 h
Result: Dose-dependently reversed the Uric acid-induced upregulation of transcription levels for inflammatory and fibrotic markers such as Nlrp3, IL-1b, Fn1 and Tgfb1.
体内研究
(In Vivo)

Ligusticum cycloprolactam (20-80 mg/kg；口服给药；每日 1 次，连续 21 天) 可通过抑制 TLR4/NF-κB 通路，降低尿酸水平、减轻肾脏炎症与纤维化，从而改善小鼠的高尿酸血症肾病[1]。

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

Animal Model: C57BL/6J (male, 8-week-old) induced by Hypoxanthine (HY-N0091) and Potassium oxonate (HY-17511)[1]
Dosage: 20, 40, 80 mg/kg
Administration: p.o.; daily; 21 days
Result: Significantly reduced serum uric acid levels and liver xanthine oxidase (XOD) activity.
Reduced kidney index, serum creatinine, blood urea nitrogen, and 24-hour albuminuria.
Ameliorated renal histological damage (decreased tubule dilation, inflammatory infiltration, and kidney injury scores).
Dose-dependently reduced macrophage infiltration.
Downregulated mRNA/protein expression of inflammatory markers (F4/80, Icam-1, IL-6, Ccl2, Nlrp3, IL-1b, MCP-1, NLRP3, IL-1β).
Decreased renal collagen deposition and downregulated fibrosis markers (Fn1, Col4a1, Tgfb1, Timp1, FN, α-SMA) while increasing E-cadherin.
Reversed dysregulation of renal uric acid transporters in the kidneys of mice.
Inhibited TLR4/NF-κB signaling, reducing TLR4 expression and p-p65 phosphorylation.
分子量

247.33

Formula

C15H21NO2
CAS 号
结构分类
初始来源
运输条件

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

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

Ligusticum cycloprolactam 相关分类

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Ligusticum cycloprolactam2283387-37-9Toll-like Receptor (TLR)NF-κBCollagenInterleukin RelatedCadherinNOD-like Receptor (NLR)Nuclear factor-κBNuclear factor-kappaBILhyperuricemic nephropathyp65NRK-52E cellsTLR4interstitial collagenTLR4/NF-κB signaling pathwaymicerenal uric acid transporterinflammatory mediatorNF-κB (p65)Inhibitorinhibitorinhibit

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