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Hanks平衡盐溶液(1×HBSS,含酚红)

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货号:AWC0157

价格:¥150

规格:500ml

  • 产品概述
  • Hanks平衡盐溶液(1×HBSS,含酚红)

    产品简介:

    平衡盐溶液(Balanced Salt Solution,BSS)与细胞生长状态下的pH值、渗透压等环境状态一致,具有维持渗透压、控制酸碱平衡、供给细胞生存代谢所必需的能量和无机盐成分等作用,可满足体外实验中细胞生存并维持一定的代谢的基本需要。主要由无机离子组成,有时含有碳酸氢钠、葡萄糖、酚红等,如果有必要还可以加入HEPES以维持渗透压的平衡。BBS配方常有改动, Hank's BBS有不含钙镁或酚红的,也有含钙镁含酚红的等,Dulbecco's PBS有不含钙镁或含钙镁的等。HBSS、EBSS、PBS等都是与较弱的磷酸盐缓冲液相关的盐溶液。常见的平衡盐溶液有Eargle's液、Hank's液、磷酸盐缓冲溶液(PBS)等。Hanks平衡盐溶液是最常用的磷酸盐缓冲溶液之一,又称Hanks' Balanced Salt Solution、Hanks' BSS、或HBSS,主要由氯化钠、氯化钾、磷酸盐、碳酸氢钠、葡萄糖等组成,含Ca2+、Mg2+ 、酚红,pH值一般为7.2~7.4。

    Hanks平衡盐溶液(1×HBSS,含酚红),含Ca2+、Mg2+、酚红,用超纯水配制,pH值7.4,经严格过滤除菌处理,内毒素含量低,可用于胰蛋白酶-EDTA细胞消化液等各种无或低钙镁细胞培养用液的配制以及组织和细胞的漂洗等,直接使用。

     

    使用方法:

    1、 无需配制,直接使用。


    注意事项:

    1、 在进行细胞培养过程中细胞的洗涤时,应注意无菌操作,避免被微生物污染。

    2、 Hanks平衡盐溶液(1×,含酚红)由于含钙离子,易产生沉淀,出现该种情况后,一般置于温浴至沉淀溶解即可,如果产生较多沉淀应弃用。

    3、 该试剂经过滤除菌。

    4、 为了您的安全和健康,请穿好实验服并佩戴一次性手套和口罩操作。

    5、 本产品仅限于专业人员的科学研究用,不得用于临床诊断或治疗,不得用于食品或药品,不得存放于普通住宅内。

    产品组成:

    名称

    货号

    规格

    storage

    Hanks平衡盐溶液1×HBSS含酚红

    AWC0157-500ml

    500ml

    4



    注意:

    1.本产品仅供科研使用。请勿用于医药、临床诊断或治疗。食品及化妆品等用途。请勿存放于普通住宅区。

    2.为了您的安全和健康,请穿好实验服并佩戴一次性手套和口罩操作。

    3.实验结果可由多种因素影响,相关处理只限于产品本身,不涉及其他赔偿。


    参考文献 (2)

    Journal of Inflammation Research IF:4.2

    Background Acute kidney injury (AKI) is associated with higher perioperative mortality and morbidity, as well as increased medical expenses. The molecular mechanisms underlying ischemia-reperfusion (I/R)-induced AKI remain unclear.Methods and Results We applied an RT-qPCR assay to measure the expression of mmu-lncRNA129814, hsa-lncRNA582795, and miRNA-494-5p, immunoblotting to detect IL-1α and cleaved caspase-3 expression, and TUNEL staining and flow cytometry (FCM) to evaluate apoptosis. The experiments were conducted using BUMPT and HK-2 cells, as well as C57BL/6J mice. Mechanistically, mmu-lncRNA129814 could sponge miRNA-494-5p and upregulate IL-1α expression to promote cell apoptosis. Furthermore, knockdown of mmu-lncRNA129814 ameliorated I/R-induced progression of AKI by targeting the miRNA-494-5p/IL-1α pathways. Interestingly, hsa-lncRNA582795, a homolog of mmu-lncRNA129814, also promoted I/R-stimulated HK-2 cell apoptosis and AKI progression by regulating the miRNA-494-5p/IL-1α axis. Finally, we found that patients with I/R-induced AKI exhibited significantly elevated plasma and urinary levels of hsa-lncRNA582795 compared to those who underwent ischemia-reperfusion without developing AKI. Spearman’s test demonstrated a significant correlation between serum creatinine and plasma hsa-lncRNA582795 in I/R patients. Plasma hsa-lncRNA582795 showed high sensitivity but low specificity (86.7%) compared to urinary hsa-lncRNA582795.Conclusion The mmu-lncRNA129814/hsa-lncRNA582795/miRNA-494-5p/IL-1α axis was found to modulate the progression of ischemic AKI, and hsa-lncRNA582795 could act as a diagnosis biomarker and potential therapy target of I/R-induced AKI.

    EXPERIMENTAL CELL RESEARCH IF:3.3

    Background Promoting muscle regeneration through stem cell therapy has potential risks. We investigated the effect of umbilical cord mesenchymal stem cells (UMSCs) Exosomes (Exo) Follistatin on muscle regeneration. Methods The Exo was derived from UMSCs cells and was utilized to affect the mice muscle injury model and C2C12 cells myotubes atrophy model. The Western blot, qRT-PCR and IF were utilized to determine the effects of Exo on the levels of Follistatin, MyHC, MyoD, Myostatin, MuRF1, MAFbx, α-SMA, Collagen I, Smad2, and AKT. In addition, HE and Masson staining were used to assess muscle tissue damage in mice. Results The level of Follistatin in Exo was significantly higher than that in UMSCs. UMSCs-Exo increased the levels of Follistatin, MyHC, MyoD, and p-Smad2 and decreased the levels of Myostatin, MuRF1, MAFbx, α-SMA, Collagen I, p-AKT, and p-mTOR in mice or C2C12 cells. In addition, UMSCs-Exo decreased levels of inflammation and fibrosis in mice. However, UMSCs-Exo-si-Follistatin reversed the effect of UMSCs-Exo. Transfection of oe-Smad2 up-regulated the protein levels of Collagen I, α-SMA, and changed the ratio of p-Smad2/Smad2 expression to 0.33, and 0.34, 0.73. LY294002 decreased the levels of MyHC, MyoD, and the ratio of p-AKT/AKT and p-mTOR/mTOR expression to 0.12, 0.17, 0.33, and 0.41, increased the levels of MuRF1 and MAFbx to 0.36 and 0.34. Conclusion This study demonstrated that Follistatin in UMSCs-Exo inhibits fibrosis and promotes muscle regeneration in mice by regulating Smad and AKT signaling.

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