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[Impacts of curcumin on proliferation, migration and cisplatin resistance of bladder cancer cells by regulating LKB1-AMPK-LC3 signaling pathway].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
January 2025
National Key Laboratory of Bioreactors, School of Biological Engineering, East China University of Science and Technology, Shanghai 200237, China. *Corresponding author, E-mail:
Article Synopsis
- The study investigates how curcumin affects bladder cancer cells regarding growth, movement, and resistance to cisplatin (a chemotherapy drug) by targeting a specific signaling pathway (LKB1-AMPK-LC3).
- Human bladder cancer cells (T24) and their cisplatin-resistant counterparts (T24/DDP) were treated with varying concentrations of curcumin, and various assays measured cell proliferation, migration, autophagy, and apoptosis.
- Results showed that curcumin, especially when combined with metformin, influences these cellular functions and could reduce drug resistance, affecting the expression of proteins in the targeted signaling pathway.
IP6K1 rewires LKB1 signaling to mediate hyperglycemic endothelial senescence.
Diabetes
January 2025
Institute for Developmental and Regenerative Cardiovascular Medicine, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.
Diabetes is a major risk factor for cardiovascular disease, but the molecular mechanisms underlying diabetic vasculopathy have been elusive. Here we report that inositol hexakisphosphate kinase 1 (IP6K1) mediates hyperglycemia-induced endothelial senescence by rewiring the liver kinase B1 (LKB1) signaling from activating the adenosine monophosphate-activated protein kinase (AMPK) pathway to the p53 pathway. We found that hyperglycemia upregulated IP6K1, which disrupts the Hsp/Hsc70 and carboxyl terminus of Hsc70-interacting protein (CHIP)-mediated LKB1 degradation, leading to increased expression levels of LKB1.
View Article and Find Full Text PDFUnlocking Therapeutic Potential: Camphorquinone's Role in Alleviating Non-Alcoholic Fatty Liver Disease via SIRT1/LKB1/AMPK Pathway Activation.
Tissue Eng Regen Med
January 2025
Department of Biological Science, College of Natural Sciences, Chosun University, 309 Pilmun-Daero, Dong-Gu, Gwangju, 501-759, Korea.
Background: Non-alcoholic fatty liver disease (NAFLD) is a pathological condition that increase the risk of simple steatosis to hepatocellular carcinoma. This study aimed to investigate the biological effects of camphorquinone (CQ) in a high-fat diet (HFD)-fed and low dose streptozotocin (STZ)-induced mouse model, widely used to mimic the concurrent development of NAFLD pathological conditions in vivo, and a free fatty acid-induced hepatic steatosis cell model in vitro.
Methods: CQ (10 or 30 mg/kg/day; i.
9-PAHSA ameliorates microvascular damage during cardiac ischaemia/reperfusion injury by promoting LKB1/AMPK/ULK1-mediated autophagy-dependent STING degradation.
Phytomedicine
November 2024
Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Hubei Key Laboratory of Biological Targeted Therapy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Hubei Provincial Engineering Research Center of Immunological Diagnosis and Therapy for Cardiovascular Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address:
Background: Considering that cardiac microvascular injury may play a more critical role than cardiomyocyte injury in the pathology of early ischaemia/reperfusion (I/R) injury, therapeutic strategies targeting the microvasculature are highly desirable. Palmitic acid-9-hydroxystearic acid (9-PAHSA) is a new class of bioactive anti-inflammatory lipids widely distributed in vegetables, fruits and medicinal plants, especially broccoli and apple. However, the pharmacological effects and underlying mechanisms of 9-PAHSA in protecting- against cardiac microvascular I/R injury have rarely been studied.
View Article and Find Full Text PDFLoureirin B Reduces Insulin Resistance and Chronic Inflammation in a Rat Model of Polycystic Ovary Syndrome by Upregulating GPR120 and Activating the LKB1/AMPK Signaling Pathway.
Int J Mol Sci
October 2024
Guangxi Key Laboratory for Applied Fundamental Research of Zhuang Medicine-Key Laboratory Project under Guangxi Health Commission, Guangxi University of Chinese Medicine, Nanning 530001, China.
Polycystic ovary yndrome (PCOS) is a common metabolic disorder in women, which is usually associated with insulin resistance (IR) and chronic inflammation. Loureirin B (LrB) can effectively improve insulin resistance and alleviate chronic inflammation, and in order to investigate the therapeutic effect of LrB on polycystic ovary syndrome with insulin resistance (PCOS-IR), we conducted animal experiments. A PCOS-IR rat model was established by feeding a high-fat diet combined with letrozole (1 mg/kg·d for 21 days).
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