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  3. TBPH

TBPH 是一种溴化阻燃剂。TBPH 在非酒精性脂肪性肝炎 (NASH) 小鼠中增强了肝脏脂肪变性、炎症和纤维化。TBPH 诱导磷脂代谢失调,降低心磷脂 (CL) 和磷脂酰丝氨酸 (PS) 水平。TBPH 导致内质网-线粒体 (ER-Mito) 接触受损,随后导致线粒体功能障碍。TBPH 通过线粒体衍生的 ds-DNA 介导的炎症反应诱导肺损伤。TBPH 可用于研究 MFN2 介导的内质网-线粒体接触在脂质代谢稳态中的作用。

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TBPH

TBPH Chemical Structure

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Customer Review

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

TBPH is a brominated flame retardant. TBPH enhances hepatic steatosis, inflammation, and fibrosis in mice with nonalcoholic steatohepatitis (NASH). TBPH induces dysregulation of phospholipid metabolism, reducing cardiolipin (CL) and phosphatidylserine (PS) levels. TBPH leads to impaired endoplasmic reticulum-mitochondria (ER-Mito) contacts, subsequently causing mitochondrial dysfunction. TBPH induces lung injury through an inflammatory response mediated by mitochondria-derived ds-DNA. TBPH can be used to study the role of MFN2-mediated ER-mitochondria contacts in lipid metabolism homeostasis[1][2].

体外研究
(In Vitro)

TBPH (5-50 μM,48 小时) 通过破坏 NASH LO 模型中 MFN2 调节的 ER-Mito 接触来促进 NASH 进展[1]
TBPH (0-20 μg/mL,48 小时) 在 TC-1 和 BEAS-2B 细胞中降低细胞增殖能力,引起氧化应激,增加肺组织纤维化,导致肺线粒体释放 ds-DNA,从而激活 c-GAS-STING[2]

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

RT-PCR[1]

Cell Line: NASH LOs model
Concentration: 5 μM, 50 μM
Incubation Time: 48 h
Result: Upregulated the transcriptional levels of oxidative stress-related genes (CYP2E1 and CYP1A2), fibrosis-related genes (COL3A1, COL4A1, LOXL2, TIMP1, VIM), and inflammation-related genes (TNF-α, IL-8).

Immunofluorescence[1]

Cell Line: NASH LOs model
Concentration: 5 μM, 50 μM
Incubation Time: 48 h
Result: Decreased colocalization of mitochondria (HSP60) and ER (GRP78), indicating reduced ER-Mito contacts.

Western Blot Analysis[1]

Cell Line: NASH LOs model
Concentration: 5 μM, 50 μM
Incubation Time: 48 h
Result: Decreased MFN2 level, increased UPRmt markers (HSP60, SOD2) and ER stress markers (GRP78, ATF6).

Western Blot Analysis[1]

Cell Line: TC-1 and BEAS-2B cells
Concentration: 0 μg/mL, 0.2 μg/mL, 2 μg/mL, 10 μg/mL
Incubation Time: 48 h
Result: Inhibited the expression of CyclinD1 and promoted the phosphorylation of Rb, increased the expression levels of CDK2/4 and P53. Increased the levels of IL-6, IL-1β, p-IκB and p-P65. Up-regulated the expression of FN and α-SMA, Down-regulated the expression of E-cadherin.
体内研究
(In Vivo)

TBPH (20-200 mg/kg,灌胃,每日一次,4 周) 在蛋氨酸胆碱缺乏 (MCD) 饮食诱导的 NASH 小鼠模型中可增强肝脏脂质蓄积和代谢功能障碍,加速肝脏炎症反应和纤维化进展,破坏肝脏磷脂稳态和肝细胞内质网-线粒体接触,诱导肝脏线粒体功能障碍和内质网应激[1]
TBPH (20-200 mg/kg,灌胃,每日一次,4 周) 在正常饮食 (ND) 小鼠模型中不会改变肝脏形态,也不会改变肝体指数,但会损害肝细胞内质网-线粒体接触,诱导的线粒体功能障碍和内质网应激[1]
TBPH(0-100 μg/mL,灌胃,每天一次,4 周)对 C57 小鼠的肺细胞造成氧化损伤,并引发肺细胞和组织的炎症反应[2]

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

Animal Model: MCD diet-induced NASH mouse (Male C57BL/6, 8-9 weeks old, 22-25 g) model[1]
Dosage: 20 mg/kg, 200 mg/kg
Administration: i.g., once a day, 4 weeks
Result: Exacerbated hepatic pathology, increased the hepatosomatic index, enhanced lipid accumulation, decreased serum HDL and CHO levels, alongside elevated hepatic TG and serum LDL levels.
Augmented hepatic steatosis and inflammatory cell infiltration, enhanced fibrotic deposition, increased steatosis, inflammatory infiltration, fibrosis and NASH scores, elevated serum levels of AST and ALT.
Reduced the abundance of cardiolipin (CL), phosphatidylserine (PS), and phosphatidylethanolamine (PE), while increasing phosphatidic acid (PA) levels.
Disrupted lipid metabolism associated with the endoplasmic reticulum and mitochondria, altered the negative intrinsic curvature of membranes.
Reduced colocalization of ER and mitochondria in liver tissues, increased the physical distance between ER and mitochondria and reduced contact sites.
Caused a marked reduction in mitochondrial cristae, disrupted cristae junctions (CJs), and disorganization of cristae membranes in hepatocytes, reduced overall oxygen consumption and ATP content.
Increased HSP60, SOD2, mitochondrial proteases (LONP1, ClpP), GRP78, Atf6, eIF2α, and Chop levels, decreased the MFN2 protein level.
Animal Model: ND mice (Male C57BL/6, 8-9 weeks old, 22-25 g) model[1]
Dosage: 20 mg/kg, 200 mg/kg
Administration: i.g., once a day, 4 weeks
Result: Did not significantly alter liver morphology, did not change the hepatosomatic index.
Affected C14:0 metabolism, fatty acids with 13-15 carbon chains, and mitochondrial metabolic processes, altered the negative intrinsic curvature of membranes.
Reduced colocalization of ER and mitochondria in liver tissues, increased the physical distance between ER and mitochondria and reduced contact sites.
Elevated the protein levels of mitochondrial chaperone HSP60, SOD2, GRP78, Atf6, eIF2α, and Chop, decreased the MFN2 protein level.
Animal Model: C57 mice model[2]
Dosage: 0 μg/mL, 0.5 μg/mL, 1 μg/mL, 5 μg/mL, 10 μg/mL, 30 μg/mL L, 60 μg/mL, 100 μg/mL
Administration: i.g., once a day, 4 weeks
Result: Induced capillary congestion in the alveolar wall and obvious inflammatory cell infiltration. Increased the expression levels of TNFα, IL-1β, IL-6, IL-8, IFNγ, eotaxin, MCP-1, MIP-2, RANTES, p16, p21, P65, and p-IκB proteins, and decreased the expression level of cell proliferation marker (Ki67). Up-regulated the expression of FN, α-SMA, and TGF-β, down-regulated the expression of E-cadherin, and increases the content of collagen fibers in the lungs. Increased ROS and MDA levels, and decreased GSH, SOD, and CAT expression levels.
分子量

708.16

Formula

C24H36Br4O4

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
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  • 稀释计算器

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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.

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