科學+家 纖維研究 | SCIENTIST HOME Fibrosis Study

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科學+家 纖維研究 | SCIENTIST HOME Fibrosis Study
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Weight: 0.25 kg

纖維化

纖維化是指各種組織的過度生長、硬化和/或瘢痕形成,並歸因於包括膠原在內的細胞外基質成分的過度沉積。纖維化是由各種刺激引起的慢性炎症反應的最終結果,包括持續感染、自身免疫反應、過敏反應、化學損傷、輻射和組織損傷。儘管現時對特發性肺纖維化、肝硬化、系統性硬化、進行性腎病和心血管纖維化等纖維化疾病的治療通常以炎症反應為目標,但越來越多的證據表明,驅動纖維化的機制不同於調節炎症的機制。事實上,一些研究表明,需要持續的炎症來逆轉已建立和進展的纖維化。纖維化的關鍵細胞介質是肌成纖維細胞,它被啟動後作為主要的膠原生成細胞。肌成纖維細胞由多種來源產生,包括上皮/內皮間充質(EMT/EndMT)轉化過程中的常駐間充質細胞、上皮細胞和內皮細胞,以及來源於骨髓幹細胞的迴圈成纖維樣細胞(稱為纖維細胞)。肌成纖維細胞被多種機制啟動,包括來自淋巴細胞和巨噬細胞的旁分泌訊號,肌成纖維細胞分泌的自分泌因數,以及與成纖維細胞上的模式識別受體(即TLR)相互作用的病原生物產生的病原體相關分子模式(PAMP)。細胞因數(IL-13,IL-21,TGF-β1),趨化因數(MCP-1,MIP-1β),血管生成因數(VEGF),生長因數(PDGF),過氧化物酶體增殖物啟動受體(PPAR),急性期蛋白(SAP),半胱天冬酶,腎素-血管緊張素-醛固酮系統(ANGⅡ)的組成部分已被確定為纖維化的重要調節因數,並被研究作為抗纖維化藥物的潜在靶點。

纖維研究

適合關注:

肺纖維化(1,2,3)

肝纖維化(4,5,13,14,15)

纖維化(6,7,16)

皮膚纖維化(8,9)

囊性纖維化(10,11)

腸道纖維化(12)

食用建议:在需要的時期,空腹食用,每日3次;每次1至3粒,250 毫升溫水飲用送服;兩餐中間或饭前 1 小时前食用。

劑形及包装:膠囊,300毫克/粒

份量:30天

產地:中國香港

重要提示:

不適用於以下情况:

  • 懷孕或哺乳期
  • 18歲以下兒童

主要成份: 蜂膠提取物、綠茶提取物、維生素D、硒、乙醯半胱氨酸


Fibrosis

Fibrosis refers to excessive growth, sclerosis and / or scarring of various tissues, and is attributed to excessive deposition of extracellular matrix components including collagen. Fibrosis is the final result of chronic inflammatory response caused by various stimuli, including persistent infection, autoimmune response, allergic reaction, chemical damage, radiation and tissue damage. Although the treatment of idiopathic pulmonary fibrosis, liver cirrhosis, systemic sclerosis, progressive kidney disease and cardiovascular fibrosis is usually aimed at inflammatory response, more and more evidence shows that the mechanism of driving fibrosis is different from that of regulating inflammation. In fact, some studies have shown that sustained inflammation is needed to reverse established and progressive fibrosis. Myofibroblasts are the key mediators of fibrosis, which are activated as the main collagen producing cells. Myofibroblasts are produced from a variety of sources, including resident mesenchymal cells, epithelial cells and endothelial cells during epithelial / endothelial mesenchymal transition (EMT / endmt), and circulating fibroblast like cells (called fibroblasts) derived from bone marrow stem cells. Myofibroblasts are activated by a variety of mechanisms, including paracrine signals from lymphocytes and macrophages, autocrine factors secreted by myofibroblasts, and pathogen associated molecular patterns (PAMPs) produced by pathogens interacting with pattern recognition receptors (TLRs) on fibroblasts. Cytokines (IL-13, IL-21, TGF - β 1), chemokines (MCP-1, MIP-1 β), angiogenic factor (VEGF), growth factor (PDGF), peroxisome proliferator activated receptor (PPAR), acute phase protein (SAP), caspase, renin angiotensin aldosterone system (Ang Ⅱ) have been identified as important regulatory factors of fibrosis, and have been widely used It has been studied as a potential target of anti fibrosis drugs.


Fibrosis Study

Suitable for attention:

  • Pulmonary fibrosis (1,2,3)
  • Liver fibrosis (4,5,13,14,15)
  • Renal fibrosis (6,7,16)
  • Skin fibrosis (8,9)
  • Cystic fibrosis (10,11)
  • Intestinal fibrosis (12)


Consumption: when necessary, 3 times a day; take 1-3 capsules each time with 250 ml warm water; take it between meals or 1 hour before meals.

Form and package: capsule, 300 mg / capsule

Portion: 30 days

Origin: Hong Kong, China

Important note:

Does not apply to:

  • Pregnancy or lactation
  • Children under 18

Main ingredients: Propolis extract, Green tea extract, Vitamin D, Selenium, Acetylcysteine.

Refs:

  1. Ming-Ju Tsai,1,2,3,4 Wei-An Chang,1,2,3 Ssu-Hui Liao,1 Kuo-Feng Chang,5 Chau-Chyun Sheu,1,2,3,4,* and Po-Lin Kuo1. The Effects of Epigallocatechin Gallate (EGCG) on Pulmonary Fibroblasts of Idiopathic Pulmonary Fibrosis (IPF)—A Next-Generation Sequencing and Bioinformatic Approach. Int J Mol Sci. 2019 Apr; 20(8): 1958.Published online 2019 Apr 22. doi: 10.3390/ijms20081958. PMCID: PMC6514693. PMID: 31013581
  2. Sriram Narayanan, Kalayarasan Srinivasan, Ganapasam Sudhandiran. Epigallocatechin-3-gallate exhibits anti-fibrotic effect by attenuating bleomycin-induced glycoconjugates, lysosomal hydrolases and ultrastructural changes in rat model pulmonary fibrosis. August 2009Chemico-biological Interactions 180(2):271-80. DOI: 10.1016/j.cbi.2009.02.017
  3. Ming-Ju Tsaim, Wei-An Chang, Ssu-Hui Liao, Kuo-Feng Chang. The Effects of Epigallocatechin Gallate (EGCG) on Pulmonary Fibroblasts of Idiopathic Pulmonary Fibrosis (IPF)—A Next-Generation Sequencing and Bioinformatic Approach. April 2019International Journal of Molecular Sciences 20(8):1958. DOI: 10.3390/ijms20081958
  4. Dong-ke Yu 1 , Cai-xia Zhang 2 , Shuang-shuang Zhao 2 , Sheng-hua Zhang 2 , Hao Zhang 2 , Shi-ying Cai 3 , Rong-guang Shao 2 , Hong-wei He 2. The anti-fibrotic effects of epigallocatechin-3-gallate in bile duct-ligated cholestatic rats and human hepatic stellate LX-2 cells are mediated by the PI3K/Akt/Smad pathway. Acta Pharmacol Sin. 2015 Apr;36(4):473-82.
    doi: 10.1038/aps.2014.155. Epub 2015 Mar 16. PMID: 25832428 PMCID: PMC4387300
  5. Ali Pezeshki1, Sara Safi2, Awat Feizi3, Gholamreza Askari1, Fatemeh Karami2. The effect of green tea extract supplementation on liver enzymes in patients with nonalcoholic fatty liver disease. DOI: 10.4103/2008-7802.173051
  6. Rattiyaporn Kanlaya and Visith Thongboonkerd. Molecular Mechanisms of Epigallocatechin-3-Gallate for Prevention of Chronic Kidney Disease and Renal Fibrosis: Preclinical Evidence. Curr Dev Nutr. 2019 Sep; 3(9): nzz101. Published online 2019 Aug 29. doi: 10.1093/cdn/nzz101. PMCID: PMC6752729. PMID: 31555758
  7. Qiang-Qiang Zhu, ORCID logo †ab Xiao-Ying Yang,†ab Xiao-Juan Zhang,†ab Cai-Jun Yu,ab Qian-Qian Pang,ab Ye-wei Huang, ORCID logo *ac Xuan-jun Wang*acd and Jun Sheng*ad. Issue 11, 2020. From the journal: Food & Function. EGCG targeting Notch to attenuate renal fibrosis via inhibition of TGFβ/Smad3 signaling pathway activation in streptozotocin-induced diabetic mice. https://doi.org/10.1039/D0FO01542C
  8. Ashwani Koul 1 , Stanzin Angmo 1 , Sanjay Bharati 2. Preventive Role of Vitamin D in Silica-Induced Skin Fibrosis: A Study in Relation to Oxidative Stress and Pro-Inflammatory Cytokines. Int J Vitam Nutr Res. 2016 Jun;86(3-4):88-96. doi: 10.1024/0300-9831/a000434. Epub 2017 Dec 8. PMID: 29219782
  9. Vira Indhiratamin Damanik1*, Imam Budi Putra2,3, Oratna Ginting2,3. Correlation between Serums 25-Hydroxyvitamin D Levels with
    Keloid Severity. ID Design Press, Skopje, Republic of Macedonia Open Access Macedonian Journal of Medical Sciences. https://doi.org/10.3889/oamjms.2019.022. eISSN: 1857-9655. Clinical Science
  10. Ruth E. Grossmann, 1 Susu M. Zughaier, 2 , 3 Meena Kumari, 4 Shabnam Seydafkan, 4 Robert H. Lyles, 5 Shuling Liu, 5 Viranuj Sueblinvong, 6 , 3 Michael S. Schechter, 2 , 7 , 3 Arlene A. Stecenko, 2 , 3 Thomas R. Ziegler, 1 , 4 and Vin Tangpricha 1 , 4 , 8 , 3 ,*. Pilot study of vitamin D supplementation in adults with cystic fibrosis pulmonary exacerbation A randomized, controlled trial. Dermatoendocrinol. Journal ListDermatoendocrinolv.4(2); 2012 Apr 1PMC3427199. 2012 Apr 1; 4(2): 191–197. doi: 10.4161/derm.20332. PMCID: PMC3427199. PMID: 22928076
  11. Supavit Chesdachai 1 , Vin Tangpricha 2. Treatment of vitamin D deficiency in cystic fibrosis. Review: J Steroid Biochem Mol Biol. 2016 Nov;164:36-39. doi: 10.1016/j.jsbmb.2015.09.013. Epub 2015 Sep 10. PMID: 26365559 PMCID: PMC4786457
  12. Qingsong Tao 1 , Baochai Wang, Yu Zheng, Xiaohua Jiang, Zheng Pan, Jianan Ren. Vitamin D prevents the intestinal fibrosis via induction of vitamin D receptor and inhibition of transforming growth factor-beta1/Smad3 pathway.
    Dig Dis Sci. 2015 Apr;60(4):868-75. doi: 10.1007/s10620-014-3398-6. Epub 2014 Oct 19. PMID: 25326845
  13. Alica Kubesch, Leonie Quenstedt, Maged Saleh, Sabrina Rüschenbaum, Katharina Schwarzkopf, Yolanda Martinez, Christoph Welsch, Stefan Zeuzem, Tania M. Welzel, Christian M. Vitamin D deficiency is associated with hepatic decompensation and inflammation in patients with liver cirrhosis: A prospective cohort study. Published: November 8, 2018. https://doi.org/10.1371/journal.pone.0207162.
  14. Kaan Demiroren, Yasar Dogan, Halil Kocamaz, Ibrahim Hanifi Ozercan. Protective effects of L-carnitine, N-acetylcysteine and genistein in an experimental model of liver fibrosis. November 2013Gastroentérologie Clinique et Biologique 38(1). DOI: 10.1016/j.clinre.2013.08.014
  15. Adil Mardinoglu 1,2,*, Dilek Ural 3, Mujdat Zeybel 4, Hatice Hilal Yuksel 1, Mathias Uhlén1 and Jan Borén 5, The Potential Use of Metabolic Cofactors in Treatment of NAFLD. Received: 1 May 2019; Accepted: 5 July 2019; Published: 12 July 2019. Nutrients 2019, 11, 1578; doi:10.3390/nu11071578
  16. Yang Shen, Nai-jun Miao, Jin-lan Xu, Xin-xin Gan, Dan Xu, Li Zhou, Hong Xue, Wei Zhang & Li-min Lu. N-acetylcysteine alleviates angiotensin II-mediated renal fibrosis in mouse obstructed kidneys. nature acta pharmacologica sinica original article. Published: 04 April 2016. Acta Pharmacologica Sinica volume 37, pages637–644(2016).