Vitamin K2 Ameliorates Diabetes-Associated Cognitive Decline by Reducing Oxidative Stress and Neuroinflammation.

IF 6.2
Kaberi Chatterjee, Anubroto Pal, Dibya Sundar Padhy, Rajdeep Saha, Amrita Chatterjee, Monika Bharadwaj, Biswatrish Sarkar, Papiya Mitra Mazumder, Sugato Banerjee
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Abstract

Diabetes, a chronic metabolic disease, affects approximately 422 million people and leads to 1.5 million deaths every year, It is found that 45% of individuals with diabetes eventually develop cognitive impairment. Here we study effects of Vitamin K2 on diabetes-associated cognitive decline (DACD) and its underlying mechanism. Diabetes was induced in adult Swiss albino mice with high-fat diet and a low dose (35 mg/kg) of streptozotocin and measured by fasting glucose and HbA1c levels. After one week of development of diabetes, one group of animals received Vitamin K2 (100 µg/kg) via oral gavage for 21 days. Then different behavioural studies, including the elevated plus maze, Morris water maze, passive avoidance test and novel object recognition test were performed followed by biochemical tests including AchE, different oxidative stress parameters (SOD, GSH, MDA, catalase, SIRT1, NRF2), inflammatory markers (TNFα, IL1β, MCP1, NFκB), apoptosis marker (Caspase 3). Hippocampal neuronal density was measured using histopathology. Vitamin K2 treatment in diabetic animals led to reduced fasting glucose and HbA1c, It could partially reverse DACD as shown by behavioural studies. Vitamin K2 adminstration reduced corticohippocampal AchE level and neuroinflammation (TNFα, IL1β, MCP1, NFκB, SIRT1). It reduced oxidative stress by increasing antioxidant enzymes (SOD, GSH, catalase), transcription factor NRF2 while reducing caspase 3. This eventually increased CA1 and CA3 neuronal density in diabetic animals. Vitamin K2 partially reverses DACD by increasing ACh while reducing the oxidative stress via Nrf2/ARE pathway and neuroinflammation, thus protecting the hippocampal neurons from diabetes associated damage.

维生素 K2 通过减少氧化应激和神经炎症改善糖尿病相关的认知功能衰退
糖尿病是一种慢性代谢性疾病,每年影响约 4.22 亿人,导致 150 万人死亡。我们在此研究维生素 K2 对糖尿病相关认知功能下降(DACD)的影响及其内在机制。用高脂肪饮食和低剂量(35 毫克/千克)链脲佐菌素诱导成年瑞士白化小鼠患糖尿病,并测量空腹血糖和 HbA1c 水平。糖尿病发生一周后,一组动物通过口服给药的方式接受维生素 K2(100 微克/千克)治疗 21 天。然后进行不同的行为研究,包括高架加迷宫、莫里斯水迷宫、被动回避测试和新物体识别测试,随后进行生化测试,包括AchE、不同的氧化应激参数(SOD、GSH、MDA、过氧化氢酶、SIRT1、NRF2)、炎症标志物(TNFα、IL1β、MCP1、NFκB)和细胞凋亡标志物(Caspase 3)。海马神经元密度通过组织病理学进行测量。对糖尿病动物进行维生素 K2 治疗可降低空腹血糖和 HbA1c,行为研究表明,维生素 K2 可部分逆转 DACD。维生素 K2 可降低皮质海马 AchE 水平和神经炎症(TNFα、IL1β、MCP1、NFκB、SIRT1)。它通过增加抗氧化酶(SOD、GSH、过氧化氢酶)和转录因子 NRF2 减少了氧化应激,同时减少了 Caspase 3。这最终增加了糖尿病动物的 CA1 和 CA3 神经元密度。维生素 K2 可通过增加 ACh 部分逆转 DACD,同时通过 Nrf2/ARE 途径和神经炎症减轻氧化应激,从而保护海马神经元免受糖尿病相关损伤。
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