1.Decidualisation of human endometrial stromal cells is associated with increased expression and secretion of prorenin.
Lumbers ER1, Wang Y1, Delforce SJ1, Corbisier de Meaultsart C1, Logan PC2,3, Mitchell MD4, Pringle KG5. Reprod Biol Endocrinol. 2015 Nov 25;13:129. doi: 10.1186/s12958-015-0127-8.
BACKGROUND: In pregnancy, the decidualised endometrium expresses high levels of prorenin and other genes of the renin-angiotensin system (RAS) pathway. In this study we aimed to determined if the RAS was present in endometrial stromal cells and if decidualisation upregulated the expression of prorenin, the prorenin receptor ((P)RR) and associated RAS pathways. Immortalised human endometrial stromal cells (HESCs) can be stimulated to decidualise by combined treatment with medroxyprogesterone acetate (MPA), 17β-estradiol (E2) and cAMP (MPA-mix) or with 5-aza-2'-deoxycytidine (AZA), a global demethylating agent.
2.Reduction of Oxidative Stress in Chronic Kidney Disease Does Not Increase Circulating α-Klotho Concentrations.
Adema AY1, van Ittersum FJ1, Hoenderop JG2, de Borst MH3, Nanayakkara PW4, Ter Wee PM1, Heijboer AC5, Vervloet MG1,6; NIGRAM consortium. PLoS One. 2016 Jan 25;11(1):e0144121. doi: 10.1371/journal.pone.0144121. eCollection 2016.
The CKD-associated decline in soluble α-Klotho levels is considered detrimental. Some in vitro and in vivo animal studies have shown that anti-oxidant therapy can upregulate the expression of α-Klotho in the kidney. We examined the effect of anti-oxidant therapy on α-Klotho concentrations in a clinical cohort with mild tot moderate chronic kidney disease (CKD). We performed a post-hoc analysis of a prospective randomized trial involving 62 patients with mild to moderate CKD (the ATIC study), all using an angiotensin-converting enzyme inhibitor (ACEi) or angiotensin receptor blocker (ARB) for 12 months. On top of that, the intervention group received anti-oxidative therapy consisting of the combination of pravastatin (40 mg/d) and vitamin E (α-tocopherol acetate, 300 mg/d) while the placebo was not treated with anti-oxidants. α-Klotho concentrations were measured at baseline and after 12 months of anti-oxidant therapy. Data were analysed using T-tests and Generalized Estimating Equations, adjusting for potential confounders such as vitamin D, parathyroid hormone, fibroblast-growth-factor 23 (FGF23) and eGFR.
3.Vinegar decreases blood pressure by down-regulating AT1R expression via the AMPK/PGC-1α/PPARγ pathway in spontaneously hypertensive rats.
Na L1, Chu X1, Jiang S1, Li C1, Li G2, He Y1, Liu Y3, Li Y4, Sun C5. Eur J Nutr. 2016 Apr;55(3):1245-53. doi: 10.1007/s00394-015-0937-7. Epub 2015 Oct 18.
PURPOSE: Vinegar has been reported to lower blood pressure, but its mechanism is unclear. This study explored whether vinegar plays antihypertensive effect by activating AMP-activated protein kinase (AMPK) pathway.
4.[Filtration of active fractions with function of expelling water retention with drastic purgative from Kansui Radix stir-baked with vinegar].
Cao LL, Wang WX, Zhang Q, Zhang L, Ding AW, Dou ZH. Zhongguo Zhong Yao Za Zhi. 2015 Sep;40(18):3655-9.
To study the function of expelling water retention with drastic purgative of different polarities of Kansui Radix stir-baked with vinegar on the cancerous ascites model rats, the furosemide was taken as positive control drug, and the cancerous ascites model rats were respectively orally administered with different polarities of Kansui Radix stir-baked with vinegar for 7 d. The amount of urine and ascites, the level of urinary sodium, potassium, chloride ion and pH, and the content of PRL1, AII, ALD in serum were investigated. Compared with model groups, ethyl acetate extract group showed a decreasing trend in ascites; the amount of urine of showed a significant increase (P < 0.05); the level of urinary sodium, potassium, chloride ion (P < 0.05, P < 0.01), pH (P < 0.05), and the content of PRL1, AII, ALD in serum all showed a significant decrease (P < 0.01). The effects of petroleum ether extract and n-butanol extract were weaker than that of ethyl acetate extract.