The protective effects of a novel polysaccharide from Lentinus edodes mycelia on islet β (INS-1) cells damaged by glucose and its transportation mechanism with human serum albumin

Cao, Xiangyu; Liú, Dan; Bi, Ruochen; He, Yonglin; Yin, He; Liu, Jianli

doi:10.1016/j.ijbiomac.2019.05.033

Cited by 27 publications

(21 citation statements)

References 68 publications

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“…Increases in TNF-α, IL-1β and IL-8 were observed in T2DM cell models, and this trend consistent with that in patients with T2DM [17]. High glucose promoted oxidative stress marker ROS and MDA production [18][19][20] and up-regulated cleaved caspase-1/3/9 and PARP-1 to induce β-cell apoptosis [19,20]. LPS enhanced β-cell apoptosis, in ammatory response and oxidative stress induced by high glucose.…”

Section: Discussionsupporting

confidence: 81%

“…Diabetes is associated with β-cell number and function failure. High glucose induces oxidative stress by increasing ROS and malondialdehyde (MDA) generation and decreasing superoxide dismutase (SOD) activity [18][19][20]. β-cell apoptosis is also induced by up-regulating cleaved caspase-1/3/9 and poly ADPribose polymerase 1 (PARP-1) [19,20].…”

Section: Introductionmentioning

confidence: 99%

“…High glucose induces oxidative stress by increasing ROS and malondialdehyde (MDA) generation and decreasing superoxide dismutase (SOD) activity [18][19][20]. β-cell apoptosis is also induced by up-regulating cleaved caspase-1/3/9 and poly ADPribose polymerase 1 (PARP-1) [19,20]. PARP-1 can weaken the DNA binding and transactivation of peroxisome proliferator activated receptor gamma (PPARγ), and CD36 decreases the transcription of the target genes of PPARγ [21].…”

Section: Introductionmentioning

confidence: 99%

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CD36 regulates β cell differentiation and influences type 2 diabetic sepsis

Liu

Shi

et al. 2021

Preprint

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Background This study aimed to investigate the diagnostic function of CD36 in type 2 diabetic (T2DM) sepsis complications (T2DSC) and its effect on β-cell differentiation. Methods First, Age - and sex-matched T2DM patients, T2DSC patients and healthy people (50 cases each) were included. Quantitative polymerase chain reaction was used to measure CD36, FOXO1, PDX1, MAFA, insulin, SOX9, Neurog3 and NANOG expression in blood samples. Second, cultured human β-cell line EndoC-βH1 and the interference and overexpression of CD36. Cell clone, apoptosis, inflammatory cytokine, oxidative stress and β-cell differentiation related proteins were also analysed. Third, examined the role of CD36 in high glucose, LPS-induced β-cell. Results CD36 mRNA, and endocrine progenitor β-cell biomarkers SOX9, Neurog3 and NANOG were significantly increased in T2DM than control group, whereas the β-cell maturation biomarkers FOXO1, PDX1, MAFA and insulin were significantly decreased. Compared with the T2DM group, CD36 and FOXO1 were significantly increased in T2DSC, but PDX1, insulin, MAFA, SOX9, Neurog3 and NANOG were significantly decreased. The receiver operating characteristic curve revealed that CD36 was useful for distinguishing T2MD and T2DSC from the control group. Furthermore, CD36 overexpression increased β-cell apoptosis and the secretion of IL-1β, IL-8 TNF-α, malondialdehyde and reactive oxygen species. CD36 induced cell defferentiation. Lastly, CD36 knockdown could inhibit the high glucose and LPS-induced cell apoptosis, inflammatory, oxidative stress and cell defferentiation. Conclusion Significant increase in CD36 can be used as a biomarker for T2MD and T2DSC. CD36 promotes T2MD or T2DSC development by inducing β-cell inflammatory and oxidative stress and defferentiation.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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CD36 regulates β cell differentiation and influences type 2 diabetic sepsis

Liu

Shi

et al. 2021

Preprint

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“…The cells (6×10 3 cell/well) were harvested and cultured in 96‐well plates overnight. Then, cells were incubated with costunolide (5, 10, 20, 30, 40 and 80 μM) for 24 and 48 h [68] . 20 μl MTT was added for 4 h, 150 μl DMSO was added when the solution was removed, and the absorbance was detected by a microplate reader (Multiskan FC, Herblain, France).…”

Section: Methodsmentioning

confidence: 99%

“…Each equal amount of cell proteins (20 μg) were loaded and separated by sodium dodecyl sulfate‐poly‐acrylamide gel electrophoresis (SDS‐PAGE) and transferred to Polyvinylidene Fluoride (PVDF) membranes by electroblotting. Then, the PVDF membranes were blocked with 5 % non‐fat milk for 1 h, and incubated with primary antibodies overnight at 4 °C [68] . The primary antibodies were used with the dilution ratio of 1 : 2000.…”

Section: Methodsmentioning

confidence: 99%

Exploring the Potential Mechanism of Costunolide‐Induced MCF‐7 Cells Apoptosis by Multi‐Spectroscopy, Molecular Docking and Cell Experiments

Liú

Zeng

et al. 2021

Chemistry & Biodiversity

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Breast cancer is one of the most common cancer with high morbidity and mortality in women. This study aimed to explore the potential mechanism of costunolide inducing MCF‐7 cells apoptosis by multi‐spectroscopy, molecular docking, and cell experiments. The results manifested that costunolide interacted with calf thymus DNA (ct‐DNA) in a spontaneous manner, and the minor groove as the preferential binding mode. Furthermore, costunolide inhibited cell proliferation and colony formation. Hoechst 33258 staining showed that cell apoptosis induced by costunolide might be related to DNA damage. The apoptosis mechanism relied on regulating the protein expression of Bax, Bcl‐2, p53, Caspase‐3 and the activation of p38MAPK and nuclear factor κB (NF‐κB) pathways. This study will provide some experimental basis and potential therapeutic strategy for breast cancer treatment.

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Potential Mechanisms of Methylglyoxal‐Induced Human Embryonic Kidney Cells Damage: Regulation of Oxidative Stress, DNA Damage, and Apoptosis

Liú

Cheng

Tang

et al. 2022

Chemistry & Biodiversity

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Methylglyoxal (MGO) is a reactive carbonyl species that can cause cellular damage and is closely related to kidney disease, especially diabetic nephropathy. The toxic effect of MGO (0.5, 1, and 2 mM) on human embryonic kidney (HEK293) cells and its underlying mechanisms were explored in this study. Cell viability, apoptosis and the signaling pathways were measured with MTT, fluorescent staining and western blot experiments, the results showed that MGO could induce oxidative stress and cell inflammation, the level of reactive oxygen species (ROS) increased, and p38MAPK, JNK and NF‐κB signaling pathways were activated. Meanwhile, MGO also induced DNA damage. The expression of DNA oxidative damage marker 8‐hydroxy‐2’‐deoxyguanosine (8‐OHdG) increased, the expression of double‐strand break marker γH2AX increased significantly, and ATM/Chk2/p53 DNA damage response signaling pathway was activated. Furthermore, the expression of the receptor for advanced glycation end products (RAGE) also increased. Finally, mitochondrial membrane potential (MMP) decreased, fluorescence intensity of Hoechst33258 increased, and the protein expression ratio of Bax/Bcl‐2 increased significantly after the treatment of MGO. These results demonstrated that MGO might induce HEK293 cells damage by regulating oxidative stress, inflammation, DNA damage, and cell apoptosis, which revealed the specific mechanisms of MGO‐induced damage to HEK293 cells.

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The protective effects of a novel polysaccharide from Lentinus edodes mycelia on islet β (INS-1) cells damaged by glucose and its transportation mechanism with human serum albumin

Cited by 27 publications

References 68 publications

CD36 regulates β cell differentiation and influences type 2 diabetic sepsis

CD36 regulates β cell differentiation and influences type 2 diabetic sepsis

Exploring the Potential Mechanism of Costunolide‐Induced MCF‐7 Cells Apoptosis by Multi‐Spectroscopy, Molecular Docking and Cell Experiments

Potential Mechanisms of Methylglyoxal‐Induced Human Embryonic Kidney Cells Damage: Regulation of Oxidative Stress, DNA Damage, and Apoptosis

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