BackgroundHyperlipidemia (HLP) presents a significant challenge to global public health. Mounting evidence suggests that statins, the recommended first-line lipid-lowering agents, have significant adverse effects. Consequently, the quest for natural and efficacious alternative therapies is steadily emerging as a research priority for HLP prevention and treatment. Consumption of tea, which is rich in diverse biologically active compounds with the capacity to regulate lipid metabolism and combat obesity, has emerged as a promising alternative therapy. Sea buckthorn leaves are rich in a multitude of biologically active substances, have a hypolipidemic effect, and can be used as a raw material for tea because of their unique flavor. There is a suggestion that combining Aspergillus cristatus with tea could modify or boost the lipid-lowering active compounds present in tea, thereby increasing its efficacy in regulating lipid metabolism.ResultsSea Buckthorn Leaf Fu Tea (SBLFT) was obtained by fermentation when sea buckthorn leaves contained 42% moisture, inoculated with Aspergillus cristatus 0.2 mL/g, and incubated for 8 d at constant temperature. Animal experiments demonstrated that SBLFT significantly inhibited body weight gain in HLP rats and reduced lipid content and serum oxidative stress. In addition, liver tissue sections and functional indices showed that SBLFT can improve liver morphology and function abnormalities. Reverse transcription-polymerase chain reaction results indicated that the expression of Liver kinase B1(LKB1), adenosine 5‘-monophosphate (AMP)-activated protein kinase(AMPK), acetyl CoA carboxylase1(ACC1), and sterol-regulatory element binding protein-1 (SREBP1c) gene related to lipid metabolism was altered.CONCLUSIONSBLFT improved HLP, specifically via promoting the expression of LKB1 in the liver of HLP rats, activating AMPK, and inhibiting ACC1 and SREBP1c expression, resulting in the inhibition of fatty acid and triglyceride synthesis-related enzymes at the transcriptional level.

The effectiveness of herbal medicine in treating diabetes has grown in recent years, but the precise mechanism by which it does so is still unclear to both medical professionals and diabetics. In traditional Chinese medicine, mulberry leaf is used to treat inflammation, colds, and antiviral illnesses. Mulberry leaves are one of the herbs with many medicinal applications, and as mulberry leaf study grows, there is mounting evidence that these leaves also have potent anti-diabetic properties. The direct role of mulberry leaf as a natural remedy in the treatment of diabetes has been proven in several studies and clinical trials. However, because mulberry leaf is a more potent remedy for diabetes, a deeper understanding of how it works is required. The bioactive compounds flavonoids, alkaloids, polysaccharides, polyphenols, volatile oils, sterols, amino acids, and a variety of inorganic trace elements and vitamins, among others, have been found to be abundant in mulberry leaves. Among these compounds, flavonoids, alkaloids, polysaccharides, and polyphenols have a stronger link to diabetes. Of course, trace minerals and vitamins also contribute to blood sugar regulation. Inhibiting alpha glucosidase activity in the intestine, regulating lipid metabolism in the body, protecting pancreatic -cells, lowering insulin resistance, accelerating glucose uptake by target tissues, and improving oxidative stress levels in the body are some of the main therapeutic properties mentioned above. These mechanisms can effectively regulate blood glucose levels. The therapeutic effects of the bioactive compounds found in mulberry leaves on diabetes mellitus and their associated molecular mechanisms are the main topics of this paper’s overview of the state of the art in mulberry leaf research for the treatment of diabetes mellitus.

目的 探讨补骨脂的反成配伍对大鼠肝脏的减毒作用及作用机制.方法 80只SD大鼠采用随机数字表法分为空白组、模型组、补骨脂组、补骨脂+制何首乌1:1组、补骨脂+制何首乌1:2组、补骨脂+制何首乌2:1组、补骨脂+熟地黄1:1组、补骨脂+五味子1:1组,每组10只大鼠.除空白组外,其他组皮下注射氢化可的松(25 mg/kg)制备肾阳虚大鼠模型,每日1次,连续注射14 d.大鼠建立肾阳虚模型后,给予相应药物干预,各组给药剂量均为12.6 g/kg,连续灌胃4周.HE染色观察大鼠肝脏组织病理变化.酶联免疫吸附测定检测大鼠血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)、碱性磷酸酶(ALP)、直接胆红素(DBIL)和总胆红素(TBIL)水平,以及肝组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)表达水平.实时荧光PCR检测核因子E2相关因子2(Nrf2)、Kelch样环氧氯丙烷相关蛋白1(Keap1)、血红素加氧酶-1(HO-1)、醌氧化还原酶1(NQO1)mRNA的表达.蛋白质印迹法检测AMP活化蛋白激酶(AMPK)/糖原合成酶激酶-3β(GSK-3β)/Nrf2信号通路中磷酸化AMP K(p-AMP K)、磷酸化GSK-3β(p-GSK-3β)、Nrf2、HO-1的蛋白表达.结果 与补骨脂组比较,补骨脂与补阴药制何首乌、熟地黄及五味子配伍后大鼠肝小叶结构改善,炎性浸润细胞减少.与补骨脂组比较,补骨脂+制何首乌1:2组、补骨脂+熟地黄1:1组、补骨脂+五味子1:1组大鼠血清中AST、ALT、ALP、DBIL、TBIL水平均降低(P<0.01);补骨脂+制何首乌1:2组大鼠肝组织SOD、GSH-Px、MDA的表达改善(P<0.01);补骨脂+制何首乌1:2组Nrf2、HO-1、NQO1 mRNA水平上调(P<0.01),Keap1 mRNA水平下调(P<0.01);补骨脂+制何首乌1:2组、补骨脂+制何首乌2:1组、补骨脂+熟地黄1:1组、补骨脂+五味子1:1组p-AMPK、p-GSK-3β、Nrf2、HO-1蛋白表达均升高(P<0.05,P<0.01).结论 补骨脂配伍补阴药制何首乌、熟地黄及五味子可改善补骨脂所致的肝损伤,其作用机制可能是通过激活AMP K/GSK-3β/Nrf2信号通路,抑制氧化应激状态来发挥对肝脏的保护作用,补骨脂与何首乌配伍比例1:2减毒效果最佳.

主要促进因子超家族结构域蛋白2a(MFSD2A)在神经系统疾病和脑血管疾病中的作用近年来日益受到关注,它被认为是突破血脑屏障的关键蛋白.MFSD2A能维持和调节血脑屏障(BBB)的完整性和通透性,对出现BBB损伤症状的多种疾病具有治疗效果,能转运二十二碳六烯酸入脑,预防和治疗阿尔茨海默病、常染色体隐性遗传原发性小头畸形等疾病;也能作为载体蛋白或调节BBB囊泡转运输送药物透过BBB治疗其他脑病.本文综述了目前MFSD2A在阿尔茨海默病、脑卒中、小头畸形等脑病中作用的研究现状,旨在为MFSD2A的基础研究和临床应用提供科学参考.

Patients received kidney transplantation (KTR) have a low seroconversion rate after vaccination. Our objective was to compare the seroconversion rates and adverse effects of additional different vaccinations in KTR patients in existing studies. Databases such as PubMed, Cochrane Library, Web of Science, Embase, ClinicalTrials.gov and others. Three high-quality RCT were included and showed no statistical difference in seroconversion rates between the two vaccines (RR = 0.93[0.76,1.13]). There was no statistical difference in seroconversion rates between the sexes, for men (RR = 0.93[0.69,1.25]) and women (RR = 0.91[0.62,1.33]). Among the adverse effects there was no statistically significant difference in fever (RR = 1.06[0.44,2.57]), while for injection site pain there was a statistically significant difference (RR = 1.14[1.18,1.84]). There was no significant difference in seroconversion rates in patients with KTR who received the two additional vaccines. Patients injected with the viral vector vaccine were less painful than those injected with the mRNA vaccine.