背景:糖尿病肾病(DN)是一种严重的糖尿病问题,可能会发展为肾衰竭。姜黄根,通常被称为姜黄,提供各种健康益处。Bisacurone是在姜黄中少量发现的生物活性萜类化合物,具有抗炎和抗氧化特性。本研究的重点是通过降低肾脏炎症对DN的潜在保护作用。氧化应激,和凋亡。
方法:2型糖尿病是通过给大鼠喂食高脂肪/高糖饮食8周来创建的,随后给予低剂量的链脲佐菌素和比沙库龙(50和100μg/kg比沙库龙),持续4周。
结果:在糖尿病大鼠中,bisacurone降低高血糖,防止体重(BW)损失,降低肾脏标志物,减少血脂改变和避免组织学异常。Bisacurone治疗通过降低丙二醛(MDA)水平降低氧化应激,同时通过超氧化物歧化酶(SOD)增强抗氧化防御,过氧化氢酶(CAT),和谷胱甘肽过氧化物酶(GPx)水平。此外,bisacurone治疗激活肾Nrf2/Keap1信号通路,但减弱高水平的NFκBp65,TNF-α,IL-1β,IL-6、Cox2和iNOS。比沙库龙也减少了Bax,caspase-3,caspase-9和细胞色素c,但增加糖尿病大鼠肾脏中的Bcl-2。
结论:在本研究中,bisacurone通过减少高血糖来减少DN,氧化应激,炎症,和细胞凋亡,同时也增加Nrf2/HO-1信令。
BACKGROUND: Diabetes nephropathy (DN) is a serious diabetic problem that may progress to renal failure. The root of Curcuma longa L., often known as turmeric, provides various health benefits.
Bisacurone is a bioactive terpenoid found in small amounts in turmeric that possesses anti-inflammatory and antioxidant properties. The present study focuses on the potential protective effects of
bisacurone against DN via reducing renal inflammation, oxidative stress, and apoptosis.
METHODS: Type 2 diabetes was created in rats by feeding them a high-fat/high-sugar diet for 8 weeks, followed by a low dose of streptozotocin and Bisacurone (50 and 100 μg/kg
bisacurone) given for 4 weeks.
RESULTS: In diabetic rats,
bisacurone reduced hyperglycemia, protected against body weight (BW) loss, lowered renal markers, reduced lipid profile alterations and avoided histological abnormalities. Bisacurone treatment reduced oxidative stress by decreasing malondialdehyde (MDA) levels while enhancing antioxidant defenses through superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) levels. Furthermore,
bisacurone treatment activated the renal Nrf2/Keap1 signaling pathway but attenuated the high levels of NFκB p65, TNF-α, IL-1β, IL-6, Cox2, and iNOS. Bisacurone also reduced Bax, caspase-3, caspase-9 and cytochrome c but increased Bcl-2 in the kidneys of diabetic rats.
CONCLUSIONS: In the present study, bisacurone reduces DN by reducing hyperglycemia, oxidative stress, inflammation, and apoptosis, while also increasing Nrf2/HO-1 signaling.