日誌
中研院說加強DcR3分子治療子宮內膜異位理論正確嗎？
中研院基因體研究中心的研究團隊今公布一項研究成果，發現DcR3分子，是造成子宮內膜細胞增強黏著力的關鍵因子，如能控制DcR3分子在子宮內膜異位中的表現，子宮內膜異症就能獲得控制
節錄自https://tw.appledaily.com/new/realtime/20171110/1238599
Decoy receptor 3 (DcR3), a member of the tumor necrosis factor (TNF) receptor (TNFR) superfamily
Decoy受體3（DcR3）是腫瘤壞死因子（TNF）受體（TNFR）超家族的成員
The experiments revealed the expression profiles of genes in RA-FLS regulated by DcR3. The profiles showed that among the 100 genes most significantly regulated by DcR3, 45 were upregulated and 55 were downregulated.
實驗揭示了DcR3調控的RA-FLS基因表達譜。圖譜顯示，在受DcR3最顯著調控的100個基因中，45個上調，55個下調。
The downregulated genes were associated with transcription regulator activity, RNA biosynthetic processes, cytoskeleton, zinc finger region, protein complex assembly, phosphate metabolic processes, mitochondrion, ion transport, nucleotide binding and cell fractionation.
下調的基因與轉錄調節活性，RNA生物合成過程，細胞骨架，鋅指區域，蛋白質複合物組裝，磷酸鹽代謝過程，線粒體，離子轉運，核苷酸結合和細胞分離有關。
節錄自https://tw.appledaily.com/new/realtime/20171110/1238599
Decoy receptor 3 (DcR3), a member of the tumor necrosis factor (TNF) receptor (TNFR) superfamily
Decoy受體3（DcR3）是腫瘤壞死因子（TNF）受體（TNFR）超家族的成員
The experiments revealed the expression profiles of genes in RA-FLS regulated by DcR3. The profiles showed that among the 100 genes most significantly regulated by DcR3, 45 were upregulated and 55 were downregulated.
實驗揭示了DcR3調控的RA-FLS基因表達譜。圖譜顯示，在受DcR3最顯著調控的100個基因中，45個上調，55個下調。
The downregulated genes were associated with transcription regulator activity, RNA biosynthetic processes, cytoskeleton, zinc finger region, protein complex assembly, phosphate metabolic processes, mitochondrion, ion transport, nucleotide binding and cell fractionation.
下調的基因與轉錄調節活性，RNA生物合成過程，細胞骨架，鋅指區域，蛋白質複合物組裝，磷酸鹽代謝過程，線粒體，離子轉運，核苷酸結合和細胞分離有關。
DcR3 binds to membrane-bound TL1A expressed on RA-FLS, resulting in the negative regulation of cell proliferation induced by inflammatory cytokines.
DcR3與RA-FLS上表達的膜結合的TL1A結合，導致由炎性細胞因子誘導的細胞增殖負調節。
子宮內膜異位、經痛，怎麼治？Part-II(如果只是經痛...同時治療內膜異位？)
所說：
前列腺素PGF2α增高，前列腺素PGE2下降時經痛疼痛加劇
PGF2α通過增加基質金屬蛋白酶 MMP-2和MMP-9來增強蛻膜明膠溶解活性
同時減少MMP-1表達的組織抑製劑。
MMP是可降解細胞外基質的水解酶之一(因此子宮內膜容易因為 MMP溶解脫落而異位 )
TIMP-2蛋白和mRNA表達由IL-4以劑量和時間依賴性方式誘導
TIMP-2表達與相應的MMP-2呈負相關。
IL-10劑量依賴性地降低MMP-9活性並增加TIMP-1水平。
就算
DcR3分子，是造成子宮內膜細胞增強黏著力的關鍵因子
可是
造成子宮內膜異位的因：前列腺素PGF2α增高以致增加基質金屬蛋白酶MMP-2和MMP-9來增強蛻膜明膠溶解活性→因此子宮內膜容易因為MMP溶解脫落而異位
的因並沒有去除
難道
只是加強DcR3分子使子宮內膜細胞增強黏著力
來對抗造成子宮內膜不斷溶解的MMP-2和MMP-9嗎？
為什麼
不補充正確營養來降低PGF2α、MMP-2和MMP-9
把造成子宮內膜異位的因去除呢？
