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咖啡莓果水萃物對小鼠腦部和肝臟之凋亡蛋白酶非依賴性細胞凋亡與自噬作用之影響

為了解決Meat GQ ptt的問題，作者林雨璇 這樣論述：

隨著年齡的增加，會因為細胞累積的損傷，造成器官受損和功能障礙。阿茲海默症(Alzheimer's disease, AD)是常見的老年退化性疾病，病理特徵為患者腦部有大量類澱粉蛋白(β-amyloid, Aβ)沉積和神經纖維纏結(neurofibrillary tangles, NFTs)，使腦神經系統退化，進而造成學習記憶功能衰退。非酒精性脂肪肝(non-alcoholic fatty liver disease, NAFLD)則是一種因脂肪囤積引起肝細胞受到破壞的疾病總稱，在老年族群亦有較高的發生率。咖啡莓果(coffeeberry, CB)是咖啡樹之果實，富含多酚類物質，具有良好的抗氧

化能力。先前本實驗室已證實咖啡莓果水萃物(coffeeberry water extract, CBWE)具有降低發炎反應、提升神經滋養因子，但其對凋亡和自噬途徑的影響尚不清楚。本研究目的為探討給予SAMP8小鼠CBWE後，透過凋亡和自噬途徑對AD和NAFLD這兩個疾病的影響。實驗選用3月齡雄性SAMP8小鼠，分為控制組、補充CBWE 10.24、20.48和40.96mg/kg BW共四組，每週紀錄體重及攝食量，為期12週。動物犧牲後測量皮質、海馬迴和肝臟中之聚腺嘌呤雙磷酸核糖聚合酶 1(poly(ADP-ribose) polymerase 1, PARP 1)、促凋亡因子(apoptos

is inducing factor, AIF)、熱休克蛋白 70(heat shock proteins 70, Hsp70)、沉默調節蛋白(silence information regulator 1, Sirt 1)、哺乳動物雷帕黴素目標蛋白(mammalian target of rapamycin, mTOR)、P70S6激酶(P70 S6 kinase, P70S6K)、自噬活化因子─Beclin 1和微管相關蛋白輕鏈3-II(microtubule-associated proteins 3-II, LC3-II)，並檢測血清生化值和肝臟抗氧化指標。結果顯示，補充CBWE能減少

皮質和海馬迴之MDA含量，此外，亦可以降低PARP 1的過度活化和裂解，並提升Hsp70的表現，因而減緩了AIF所產生的細胞毒性，進而抑制細胞凋亡的現象；CBWE亦可增加Sirt 1的表現，減少了mTOR和P70S6K的磷酸化，提升了Beclin 1和LC3-II之蛋白表現，進而促進自噬作用。此外，CB在肝臟組織可降低脂質和蛋白質的氧化，抑制細胞凋亡和促進自噬作用的相關蛋白表現，進而有效改善肝功能指標。綜合以上，CBWE可降低氧化壓力和凋亡因子的表現，增加自噬因子的產生，可能藉此延緩年齡增長所造成可能的細胞損傷。

Genetic Polymorphisms Associated with Colorectal Cancer in Patients with Lynch Syndrome in Taiwan

為了解決Meat GQ ptt的問題，作者Abram Bunya Kamiza 這樣論述：

ABSTRACTBackgroundLynch syndrome is an autosomal dominant disorder caused by germline mutation in mismatch repair (MMR) genes. Patients with Lynch syndrome have an increased risk of developing colorectal cancer (CRC) and other Lynch syndrome-related cancers including cancer of the endometrium, ovar

y, brain, bladder, prostate, renal pelvis, small bowel, hepatobiliary tract, and stomach.Study objectivesThe overall aim of this study was to determine genetic polymorphisms that are associated with CRC in patients with Lynch syndrome in Taiwan, and we have three specific objectives to achieve our a

im.1. To estimate the age-and sex-specific cumulative risk of developing CRC in patients with Lynch syndrome in Taiwan.2. To investigate whether polymorphisms of xenobiotic-metabolizing genes, DNA repair genes, TP53 gene, and TGFB pathway genes are associated with CRC.3. To investigate whether xe

nobiotic-metabolizing genes interact with environmental factors to modify CRC risk in patients with Lynch syndrome.Material and methodsPatients suspected of having hereditary non-polyposis colorectal cancer where recruited into the Amsterdam criteria family registry using the Amsterdam II criteria.

Probands and family members who met the criteria were screened for germline mutation in MLH1 and MSH2. Genotyping of xenobiotic-metabolizing genes, DNA repair genes, TP53 gene, and TGFB pathways genes were performed using Sequenom iPLEX MassARRAY. Age-and sex-specific cumulative risk of CRC in patie

nts with Lynch syndrome were calculated using Mendel version 16. A weighted Cox proportional hazard model was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for association between genetic polymorphisms and CRC. Multiplicative interactions between xenobiotic-metabolizing ge

nes and environmental factors were assessed by likelihood ratio test.ResultsAge-specific cumulative risk of CRC in patients with Lynch syndrome at age 70 were estimated to be 29.3% (95% CI, 23.6%–36.5%) for MLH1 or MH2, 27.5% (95% CI, 22.0%–34.0%) for MLH1, and 36.8% (95% CI, 28.4%–46.7%) for MSH2

germline mutation. Variant TT and CC genotypes of xenobiotic-metabolizing genes GSTA1 rs3957356 (HR = 5.36, 95% CI = 2.39–12.0) and CYP1B1 rs1056836 (HR = 7.24, 95% CI = 3.51–14.9) significantly increased the risk of CRC compared with the wild-type CC and GG genotypes, respectively. For DNA repair g

enes, the heterozygous variants of rs1799832 in NUDT1 (HR = 2.97, 95% CI = 1.51–5.83) and rs13181 in ERCC2 (HR = 2.69, 95% CI = 1.10–6.55) also significantly increased the risk of CRC compared with wild-type homozygous CC and TT genotypes, respectively. Patients carrying the AA genotype of EGFR rs22

27983 had a higher risk of CRC (HR = 2.55, 95% CI = 1.25–5.17) than those carrying the G allele. Moreover, the dominant model of SMAD7 rs12953717 significantly increased CRC risk (HR = 2.17, 95% CI = 1.12–4.16) compared with the wild-type CC genotype. However, CYP1A1 rs4646903 CC genotype was associ

ated with a decrease risk of CRC (HR = 0.33, 95% CI = 0.12–0.89) compared with the TT genotype. The GC+GG genotype in MUTYH rs3219489 of DNA repair exerted a protective effect (HR = 0.49, 95% CI = 0.26–0.91) compared with the CC genotype. The variant C allele of TP53 rs1042522 were associated with a

decreased CRC risk (HR = 0.35, 95% CI = 0.14–0.86 and HR = 0.28, 95% CI = 0.13–0.57 for GC and CC genotypes, respectively). Similarly, the CT (HR = 0.20, 95% CI = 0.08–0.46) and the TT (HR = 0.25, 95% CI = 0.09–0.65) genotypes of the TP53 rs12947788 also significantly decreased CRC risk. Moreover,

we found significant interaction between polymorphisms in xenobiotic-metabolizing genes and intake of meat.ConclusionAge-specific cumulative risk of CRC in Chinese patients with Lynch syndrome were estimated to be 27.5% for MLH1 and 36.8% for MSH2 mutation carriers after adjusted for ascertainment b

ias. Polymorphisms in GSTA1 rs3957356, CYP1B1 rs1056836, NUDT1 rs1799832, ERCC2 rs13181, EGFR rs2227983, and SMAD7 rs12953717 were significantly associated with an increased risk of CRC, whereas polymorphisms in CYP1A1 rs4646903, MUTYH rs3219489, TP53 rs1042522, and rs12947788 were associated with a

decreased CRC risk.