我们的研究旨在通过调节蛋白质精氨酸N-甲基转移酶1-不对称二甲基精氨酸-二甲基精氨酸-二甲基精氨酸二甲基氨基水解酶(PRMT1-DDAH-ADMA)与雷帕霉素-Sirtuin1-5\'AMP活化蛋白激酶(mTOR-SIRT1)和AMPRT1途径的哺乳动物靶标,分析来自外消旋茎的硫酸多糖(SPCr)在减轻肥胖诱导的心脏代谢综合征中的这是一项后续研究,使用了以前体外研究的SP,由2,3-二-O-甲基-1,4,5-三-O-乙酰阿拉伯糖醇组成,2,3,4,6-四-O-甲基-D-吡喃甘露糖,和B型ulvanobionicacid3-硫酸盐。将40只大鼠随机分为四个治疗组:A组接受标准饮食;B组提供富含胆固醇和脂肪的饮食(CFED);C组和D组给予CFED以及随意饮水,和每日口服补充65或130毫克/千克体重(BW)的SPCr,分别。D组低密度脂蛋白最低,甘油三酯,总胆固醇,和血糖水平,与本研究中的其他组相比,HDL水平最高。与饲喂低剂量SPCr的组相比,饲喂高剂量SPCr的组的这些结果证明了显着的效果(p<0.0001),以及总胆固醇和血糖(p<0.05)。还观察到补充SPCr对过氧化物酶体增殖物激活受体γ辅激活因子(PGC)-1α有上调作用,白介素10,Sirtuin1,DDAH-II,超氧化物歧化酶(SOD)心脏,和AMPK,随后还下调了PRMT-1,TNF-α,3-羟基-3-甲基戊二酰辅酶A还原酶抑制剂,还有MTOR.有趣的是,还观察到肠道微生物群调节;用富含胆固醇的饮食喂养大鼠,使肠道微生物群组成向Firmicutes水平转移,降低了拟杆菌的水平,并提高了Firmicutes水平。推荐剂量为130mg/kgBW的SPCr,和研究仍需继续在临床试验与人类看到其疗效在先进水平。
Our investigation intended to analyze the effects of sulfated polysaccharides from Caulerpa racemosa (SPCr) in attenuating obesity-induced cardiometabolic syndrome via regulating the protein arginine N-methyltransferase 1-asymmetric dimethylarginine-dimethylarginine dimethylamino-hydrolase (PRMT1-DDAH-ADMA) with the mammalian target of rapamycin-Sirtuin 1-5\' AMP-activated protein kinase (mTOR-SIRT1-AMPK) pathways and gut microbiota modulation. This is a follow-up study that used SPs from previous in vitro studies, consisting of 2,3-di-O-methyl-1,4,5-tri-O-acetylarabinitol, 2,3,4,6-tetra-O-methyl-D-mannopyranose, and type B ulvanobiuronicacid 3-sulfate. A total of forty rats were randomly divided into four treatment groups: Group A received a standard diet; Group B was provided with a diet enriched in cholesterol and fat (CFED); and Groups C and D were given the CFED along with ad libitum water, and daily oral supplementation of 65 or 130 mg/kg of body weight (BW) of SPCr, respectively. Group D showed the lowest low-density lipoprotein, triglyceride, total cholesterol, and blood glucose levels, and the highest HDL level compared to the other groups in this study. These results in the group fed high-dose SPCr demonstrated a significant effect compared to the group fed low-dose SPCr (p < 0.0001), as well as in total cholesterol and blood glucose (p < 0.05). Supplementation with SPCr was also observed to have an upregulation effect on peroxisome proliferator-activated receptor gamma coactivator (PGC)-1alpha, interleukin 10, Sirtuin 1, DDAH-II, superoxide dismutase (SOD) cardio, and AMPK, which was also followed by a downregulation of PRMT-1, TNF-α, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, and mTOR. Interestingly, gut microbiota modulation was also observed; feeding the rats with a cholesterol-enriched diet shifted the gut microbiota composition toward the Firmicutes level, lowered the Bacteroidetes level, and increased the Firmicutes level. A dose of 130 mg/kg BW of SPCr is the recommended dose, and investigation still needs to be continued in clinical trials with humans to see its efficacy at an advanced level.