Lipoic acid is an organosulfur compound which is essential for aerobic metabolism.
Also known as α-lipoic acid (α-LA), alpha lipoic acid (ALA) and thioctic acid.
Alpha-lipoic acid (ALA) is synthesized enzymatically in human cells and regulates the mitochondrial enzymes as cofactor.
ALA improved the anticancer potential of several NSAIDs. (NSAIDs can stimulate apoptosis and inhibit angiogenesis, and reduce tumor growth)
α-Lipoic Acid is a therapeutic agent against neuroinflammatory responses.
Alpha-Lipoic Acid has been suggested to have anti-dementia and anti-Alzheimer’s Disease properties due to several actions, such as scavenging the reactive oxygen species (ROS), reducing inflammatory processes, and regenerating endogenous antioxidants.
Metal Chelating Activity
Disease / Symptom Treatment
Alpha Lipoic Acid improved the anticancer potential of several NSAIDs when tested against human gioblastoma cell lines.
Alpha Lipoic Acid is well known to exert its antitumor activities in different cell lines by apoptosis-mediated mechanisms.[1:1]
ALA improved the anticancer potential of several NSAIDs. (NSAIDs have been shown to stimulate apoptosis and inhibit angiogenesis, and reduce tumor growth).[1:2]
Title: Metformin or α-Lipoic Acid Attenuate Inflammatory Response and NLRP3 Inflammasome in BV-2 Microglial Cells
Publication: Korean Journal of Clinical Laboratory Science
Date: September 2020
Study Type: Animal Study, Commentary, Human Study: In Vitro - In Vivo - In Silico, Human: Case Report, Meta Analysis, Review
Author(s): Hye-Rim Choi, Ji Sun Ha, In Sik Kim, Seung-Ju Yang
Institution(s): Konyang University, Daejeon, Korea
Abstract: Alzheimer’s disease (AD) is a chronic and progressive neurodegenerative disease that can be described by the occurrence of dementia due to a decline in cognitive function. The disease is characterized by the formation of extracellular and intracellular amyloid plaques. Amyloid beta (Aβ) is a hallmark of AD, and microglia can be activated in the presence of Aβ. Activated microglia secrete pro-inflammatory cytokines. Furthermore, S100A9 is an important innate immunity pro-inflammatory contributor in inflammation and a potential contributor to AD. This study examined the effects of metformin and α-LA on the inflammatory response and NLRP3 inflammasome activation in Aβ- and S100A9-induced BV-2 microglial cells. Metformin and α-LA attenuated inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). In addition, metformin and α-LA inhibited the phosphorylation of JNK, ERK, and p38. They activated the nuclear factor kappa B (NF-κ B) pathway and the NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome. Moreover, metformin and α-LA reduced the marker levels of the M1 phenotype, ICAM1, whereas the M2 phenotype, ARG1, was increased. These findings suggest that metformin and α-LA are therapeutic agents against the Aβ- and S100A9-induced neuroinflammatory responses.
Title: Anticancer effects of novel NSAIDs derivatives on cultured human glioblastoma cells
Publication: Zeitschrift für Naturforschung C
Date: September 2020
Study Type: Human Study: In Vitro
Author(s): Özlem Özdemir, Lisa Marinelli, Ivana Cacciatore, Michele Ciulla, Bugrahan Emsen, Antonio Di Stefano, Adil Mardinoglu, and Hasan Turkez
Institution(s): King’s College, London; G. D’Annunzio University, Chieti, Italy; Atatürk University, Erzurum, Turkey; Karamanoğlu Mehmetbey University, Karaman, Turkey
Abstract: Several epidemiologic, clinical and experimental reports indicate that nonsteroidal anti-inflammatory drugs (NSAIDs) could have a potential as anticancer agents. The aim of this study was the evaluation of cytotoxic potential in human glioblastoma cells of novel synthesized NSAID derivatives, obtained by linking, through a spacer, α-lipoic acid (ALA) to anti-inflammatory drugs, such as naproxen (AL-3, 11 and 17), flurbiprofen (AL-6, 13 and 19) and ibuprofen (AL-9, 15 and 21). The effects on the level of gene expression were also determined using quantitative real-time polymerase chain reaction (qRT-PCR) analysis. According to our results, NSAID derivatives exhibited concentration dependent cytotoxic effects on U87-MG cell line when compared with the control group. Moreover, treatment of the most active compounds (AL-3, AL-6 and AL-9) caused upregulation of tumor suppressor gene PTEN and downregulation of some oncogenes such as AKT1, RAF1 and EGFR. In conclusion, our results revealed that AL-3, AL-6 and AL-9 could be suitable candidates for further investigation to develop new pharmacological strategies for the prevention of cancer.