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MIN6

Cat.No.: CSC-C9215W

Species: Mouse

Source: pancreas

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Cat.No.
CSC-C9215W
Description
MIN6 cells excreted insulin, glucagon, somatostatin and ghrelin.
Species
Mouse
Source
pancreas
Recommended Medium
Storage and Shipping
liquid nitrogen vapor phase
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

The MIN6 mouse insulinoma cell line is derived from an insulinoma tissue developed in a transgenic mouse in which the human insulin promoter drives the expression of the Simian Virus 40 Large T antigen. In comparison to primary pancreatic beta cells, MIN6 mouse insulinoma cell line grows more robustly and more vigorously in cell culture, while retaining important features of beta cells, such as the exclusive expression of the so-called "liver-type" glucose transporter (Glut2) and their ability to modulate insulin secretion in response to changes in glucose concentration in the growth medium, and it has been a staple strain in diabetes research since its establishment in 1990. In addition, the expression of the major histocompatibility complex I (MHC I) is lacking in MIN6, as in the non-diabetic beta cells, but can be induced by proinflammatory cytokines, which would render them susceptible to T-cell mediated cytotoxicity. This closely mimics the behavior of beta cells isolated from diabetic tissues, where chronic inflammation is commonly observed, and it has made MIN6 an attractive cell line model for investigating the mechanism of beta cell loss due to their autoimmune destruction.

Nickel Sulfate Induced GSIS Injury in MIN6 Cells by Activating the JNK Pathway Through Oxidative Stress

Nickel has an impact on human health, especially in the context of new energy industries. Nickel's influence on glycemia remains controversial, and the effect and mechanism of nickel on islet function still need further exploration.

MIN6 cells were treated with different concentrations of nickel sulfate (NiSO4) (0, 75, 150, and 300 µg/mL) for different durations (0, 12, 24, and 48 h). The study measured cell cycle progression, apoptosis, reactive oxygen species (ROS) production, oxidative stress–related indexes (T-SOD, TBARS, 8-OHdG, and GSH), glucose-induced insulin secretion (GSIS), and the expression of JNK pathway–related proteins, pancreaticoduodenal homeobox-1 (PDX-1), glucose transporter 2 (GLUT2), and forkhead box protein O1 (FOXO1). NiSO4 damaged MIN6 cells in a time- and dose-dependent manner. NiSO4 blocked the cell cycle, induced apoptosis, and reduced insulin secretion in the GSIS experiment. NiSO4 also induced ROS production, increased oxidative stress–related indexes (TRABS and 8-OHdG), and decreased antioxidant stress–related indexes (GSH and T-SOD). In addition, NiSO4 activated the JNK pathway, upregulated FOXO1 protein expression, and inhibited PDX-1 and GLUT2 protein expression, affecting insulin release during GSIS.

NiSO4 reduced the viability of MIN6 cells, blocked the cell cycle in the G0/G1 phase, induced cell apoptosis, and caused damage to the islet cell function.Fig. 1. NiSO4 reduced the viability of MIN6 cells, blocked the cell cycle in the G0/G1 phase, induced cell apoptosis, and caused damage to the function of islet cells (Sun, Bo, and Hui Chen. 2024).

NiSO4 activated JNK pathway in MIN6 cells by inducing oxidative stress, upregulated FOXO1 protein expression, and downregulated PDX-1 and GLUT2 protein expression, affecting insulin release during GSIS.Fig. 2. NiSO4 activated the JNK pathway, upregulated FOXO1 protein expression, and inhibited PDX-1 and GLUT2 protein expression, resulting in decreased GSIS function of MIN6 cells (Sun, Bo, and Hui Chen. 2024).

Puerarin Ameliorates High Glucose-Induced MIN6 Cell Injury by Activating PINK1/Parkin-Mediated Mitochondrial Autophagy

The dysfunction of pancreatic β-cells plays a key role in the pathogenesis of type 2 diabetes mellitus (T2DM). Despite numerous studies have demonstrated the anti-inflammatory and antioxidant properties of puerarin, the protective effects of puerarin on β-cells remain poorly understood. Hence, this study aimed to explore the effects of puerarin on β-cell dysfunction in a hyperglycemic environment via the PINK/Parkin-mediated mitochondrial autophagy pathway.

MIN6 cells were exposed to glucose concentrations of 5 mM, 10 mM, 20 mM, and 30 mM for 24 h, 48 h, and 72 h, respectively. Results indicated a significant decrease in MIN6 cell viability following 48 h of exposure to 30 mM glucose concentration. Puerarin intervention markedly attenuated ROS production, restored mitochondrial membrane potential, induced PINK/Parkin-mediated mitochondrial autophagy, suppressed activation of the mitochondrial apoptotic pathway, mitigated apoptosis, and enhanced insulin secretion in a high glucose (HG) environment. The findings of this investigation contribute to a deeper understanding of the precise mechanism underlying the protective effects of puerarin on β-cells and offer a theoretical foundation for advancing puerarin-based therapeutics aimed at ameliorating T2DM.

The effects of hypertonic conditions, high glucose (HG), and DMSO on the viability of MIN6 cells.Fig. 3. Effect of different concentrations of glucose and time on the viability values of MIN6 cells (Zhu, Hongyang, et al. 2024).

RT-qPCR and western blot detection of PINK1, Parkin, Beclin-1, p62 and LC3II mRNA and protein expression levels in MIN6 cells.Fig. 4. Puerarin enhances PINK1/Parkin-mediated mitochondrial autophagy in HG-induced MIN6 cells (Zhu, Hongyang, et al. 2024).

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