Curcumin suppresses AGEs induced apoptosis in tubular epithelial cells via protective autophagy

Wei, Ying; Gao, Jiaqi; Qin, Lingling; Xu, Yunling; Shi, Haoxia; Qu, Ling-Xia; Liu, Yongqiao; Tian, Xu; Liu, Tonghua

doi:10.3892/etm.2017.5314

Cited by 14 publications

(18 citation statements)

References 25 publications

(22 reference statements)

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“…Previous researches have shown that high glucose promoted autophagy in endothelial cells by inhibiting PI3K/AKT signaling [ 7 ]. While in RPE cells, autophagy can prevent the oxidative damage caused by diabetes [ 22 ]. We have revealed that autophagy has a positive effect on RPEs under intermittent high glucose condition.…”

Section: Discussionmentioning

confidence: 99%

Intermittent high glucose-induced oxidative stress modulates retinal pigmented epithelial cell autophagy and promotes cell survival via increased HMGB1

Zhang¹,

Song²,

Zhang³

et al. 2018

BMC Ophthalmol

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BackgroundIn this study, we evaluated the effects of intermittent high glucose on oxidative stress production in retinal pigmented epithelial (RPE) cells and explored whether the mechanisms of autophagy and apoptosis in oxidative stress are associated with high-mobility group box 1 (HMGB1) protein.MethodsCultured human RPE cell line ARPE-19 cells were exposed to intermittent high glucose-induced oxidative stress. Reactive oxygen species (ROS) was determined by 2′, 7′-dichlorofluorescin diacetate (DCFH-DA); and malonyldialdehyde (MDA), superoxide dismutase (SOD) by commercial kits. Transmission electron microscopy was used to observe the generation of autophagosome. And MTT assay was used to examine the effect of autophagy on cell viability. For the inhibition experiments, cells were pre-incubated with lysosomal inhibitors NH4Cl or N-acetyl cysteine (NAC).Western blot was used to measure the expression patterns of autophagic markers, including LC3 and p62. The expression of HMGB1 was detected by immunohistochemistry.Cells were pre-incubated with HMGB1 inhibitor ethyl pyruvate (EP) ,then detected the expression pattern of autophagic markers and level of cellular ROS.ResultsWe found that intermittent high glucose significantly increased oxidative stress levels (as indicated by ROS, MDA, SOD), increased in the generation of autophagosome, decreased the level of p62, induced conversion of LC3 I to LC3 II. We further demonstrated that the NH4Cl/NAC inhibited intermittent high glucose-induced autophage by altered level of LC3 and p62. Intermittent high glucose-induced autophagy is independent of HMGB1 signaling, inhibition of HMGB1 release by EP decreased expression pattern of autophagic markers and level of cellular viability.ConclusionsUnder intermittent high glucose condition, autophagy may be required for preventing oxidative stress-induced injury in RPE. HMGB1 plays important roles in signaling for both autophagy and oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Intermittent high glucose-induced oxidative stress modulates retinal pigmented epithelial cell autophagy and promotes cell survival via increased HMGB1

Zhang¹,

Song²,

Zhang³

et al. 2018

BMC Ophthalmol

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“…Astilbin [140], astragaloside IV [15], curcumin [41], Psoralea corylifolia [115], quercetin [49], secoisolariciresinol diglucoside [88], silybin [43], berberine [45], berberine [44], berberine [136], tripterygium glycosides [138], celastrol [170], curcumin [132], resveratrol [133], astragaloside IV [103], Cyclocarya paliurus-triterpenic acids-enriched fraction [142], ferulic acid [145]…”

Section: Apoptosismentioning

confidence: 99%

“…Astilbin [140], astragaloside IV [15], emodin [94], Hypericum perforatum [31], berberine [45], berberine [44], curcumin [132], resveratrol [133], resveratrol [168], astragaloside IV [103], Cyclocarya paliurus-triterpenic acids-enriched fraction [142] Tangshen Formula [123] Collagen 4…”

Section: Hif-1α/pi3k/aktmentioning

confidence: 99%

“…By degrading damaged cellular components, autophagy, an adaptive response of cells exposed to various environmental stresses, is essential for maintaining the structural and functional well-being of podocytes [ 103 , 131 , 132 ]. Consequently, its malfunction in DN leads to podocyte loss and proteinuria [ 133 ].…”

Section: Herbal Nephroprotectionmentioning

confidence: 99%

“…Several pathways converge in regulating autophagy and are the points of impact of the various herbal products that enhance cell viability by activating autophagy: AMPK (berberine [ 136 ]), mTOR (hispidulin [ 137 ]), PI3K/AKT (curcumin [ 132 ]), and β -arrestin-1 (tripterygium glycosides [ 138 ]). Besides increasing autophagy, celastrol also dampens inflammation, oxidative stress, and apoptosis and hence increases podocyte viability, as reflected by enhanced expression of nephrin [ 139 ].…”

Section: Herbal Nephroprotectionmentioning

confidence: 99%

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Mechanisms of Herbal Nephroprotection in diabetes mellitus

Dragoș

Manea

Timofte

et al. 2020

Journal of Diabetes Research

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Diabetic nephropathy (DN) is a leading cause of kidney morbidity. Despite the multilayered complexity of the mechanisms involved in the pathogenesis of DN, the conventional treatment is limited to just a few drug classes fraught with the risk of adverse events, including the progression of renal dysfunction. Phytoceuticals offer a promising alternative as they act on the many-sidedness of DN pathophysiology, multitargeting its intricacies. This paper offers a review of the mechanisms underlying the protective action of these phytoagents, including boosting the antioxidant capabilities, suppression of inflammation, averting the proliferative and sclerosing/fibrosing events. The pathogenesis of DN is viewed as a continuum going from the original offense, high glucose, through the noxious products it generates (advanced glycation end-products, products of oxidative and nitrosative stress) and the signaling chains consequently brought into action, to the harmful mediators of inflammation, sclerosis, and proliferation that eventually lead to DN, despite the countervailing attempts of the protective mechanisms. Special attention was given to the various pathways involved, pointing out the ability of the phytoagents to hinder the deleterious ones (especially those leading to, driven by, or associated with TGF-β activation, SREBP, Smad, MAPK, PKC, NF-κB, NLRP3 inflammasome, and caspase), to promote the protective ones (PPAR-α, PPAR-γ, EP4/Gs/AC/cAMP, Nrf2, AMPK, and SIRT1), and to favorably modulate those with potentially dual effect (PI3K/Akt). Many phytomedicines have emerged as potentially useful out of in vitro and in vivo studies, but the scarcity of human trials seriously undermines their usage in the current clinical practice—an issue that stringently needs to be addressed.

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