Berberine protects human renal proximal tubular cells from hypoxia/reoxygenation injury via inhibiting endoplasmic reticulum and mitochondrial stress pathways

Yu, Wenli; Sheng, Mingwei; Xu, Rubin; Yu, Jianjian; Cui, Kang; Tong, Jingkai; Shi, Libin; Ren, Hengchang; Du, Hongyin

doi:10.1186/1479-5876-11-24

Cited by 98 publications

(73 citation statements)

References 37 publications

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“…25 In parallel, two ER stress hallmarks, GRP78 and CHOP, showed increased protein levels after hypoxia and ER stress, and participated in hypoxia/reoxygenation induced apoptosis in human renal proximal tubular epithelial cell line (HK-2 cells). 49 However, those parameters were significantly suppressed by berberine pretreatment. 49 It was also demonstrated that tauroursodeoxycholic acid (TUDCA) pretreatment had a nephroprotective effect on ischemia-induced AKI by inhibiting ER stress and by blocking GRP78 and CHOP expression, reducing Caspase 12 activation, and inhibiting cell apoptosis.…”

Section: Apoptosis Promoting Effect Of Er Stress and Interventionsmentioning

confidence: 83%

“…49 However, those parameters were significantly suppressed by berberine pretreatment. 49 It was also demonstrated that tauroursodeoxycholic acid (TUDCA) pretreatment had a nephroprotective effect on ischemia-induced AKI by inhibiting ER stress and by blocking GRP78 and CHOP expression, reducing Caspase 12 activation, and inhibiting cell apoptosis. 48 There are other interventions being explored.…”

Section: Apoptosis Promoting Effect Of Er Stress and Interventionsmentioning

confidence: 83%

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Endoplasmic reticulum stress and its effects on renal tubular cells apoptosis in ischemic acute kidney injury

Guo

Jiang

et al. 2016

Renal Failure

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Ischemia is the most frequent cause of acute kidney injury (AKI), which is characterized by apoptosis of renal tubular cell. A common result of ischemia in AKI is dysfunction of endoplasmic reticulum (ER), which causes the protein-folding capacity to lag behind the protein-folding load. The abundance of misfolded proteins stressed the ER and results in induction of the unfolded protein response (UPR). While the UPR is an adaptive response, over time it can result in apoptosis when cells are unable to recover quickly. Recent research suggests that ER stress is a major factor in renal tubular cell apoptosis resulting from ischemic AKI. Thus, ER stress may be an important new progression factor in the pathology of ischemic AKI. In this article, we review UPR signaling, describe pathology and pathophysiology mechanisms of ischemic AKI, and highlight the dual function of ER stress on renal tubular cell apoptosis. ARTICLE HISTORY

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Section: Apoptosis Promoting Effect Of Er Stress and Interventionsmentioning

confidence: 83%

Section: Apoptosis Promoting Effect Of Er Stress and Interventionsmentioning

confidence: 83%

Endoplasmic reticulum stress and its effects on renal tubular cells apoptosis in ischemic acute kidney injury

Guo

Jiang

et al. 2016

Renal Failure

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“…In addition, the anti-apoptotic potential of berberine against renal injury is in agreement with the previous findings. 81 …”

Section: Discussionmentioning

confidence: 99%

Ameliorative effect of berberine against gentamicin-induced nephrotoxicity in rats via attenuation of oxidative stress, inflammation, apoptosis and mitochondrial dysfunction

et al. 2016

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Background: Gentamicin (GM) is the commonly used antibiotics against Gram-negative infection, but the nephrotoxic potential of drug limit its clinical interest. The aim of this study was to investigate the protective effect of berberine (BER) against GM-induced nephrotoxicity and possible underlying mechanisms. Material and methods: The rats were divided into various group, namely normal, GM-control, GM þ BER (10, 20, and 40 mg/kg). Nephrotoxicity was induced by intraperitoneal administration of GM (120 mg/kg) for 7 consecutive days. BER (10, 20, and 40 mg/kg; p.o.) was also administered for the 7 days. Various biochemical, molecular, and histological parameters were assessed in serum and kidney. Results: GM-administration significantly increased (p < 0.001) the serum creatinine and blood urea nitrogen (BUN) as well as renal malonaldehyde (MDA), nitric oxide (NO) along with Kidney Injury Molecule-1 (KIM-1), Neutrophil gelatinase-associated lipocalin (NGAL), and nuclear factor-kappa B (NF-KB) renal mRNA expressions. In addition, GM also significantly decreased (p < 0.001) the renal superoxide dismutase (SOD), reduced glutathione (GSH), B-cell lymphoma 2 (Bcl-2) mRNA expression, and mitochondrial enzymes (NADH dehydrogenase and cytochrome c oxidase) activities. Rats treated with BER (20 and 40 mg/kg; p.o.) significantly and dose-dependently (p < 0.05 and p < 0.01) restore the altered levels of antioxidant, inflammatory, apoptosis, AKI markers as well as depleted mitochondrial enzymes. Histopathological abbreviations were also ameliorated by BER administration. Conclusion: Berberine exerts renoprotective effects through its anti-oxidant, anti-inflammatory, and anti-apoptotic properties.

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“…[159] . Berberine has been reported to ameliorate proinflammatory cytokine-induced ERS in human intestinal epithelial cells [160] , reduce hypoxia/reoxygenation-induced human renal proximal tubular cell injury [161] , and inhibit the human immunodeficiency virus protease inhibitor-induced inflammatory response in murine macrophages [162] . Berberine has also been suggested to have an anti-hypertensive property [163] .…”

Section: Endoplasmic Reticulum Stress Is Involved In the Development mentioning

confidence: 99%

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

2016

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Endoplasmic reticulum is a principal organelle responsible for folding, post-translational modifications and transport of secretory, luminal and membrane proteins, thus palys an important rale in maintaining cellular homeostasis. Endoplasmic reticulum stress (ERS) is a condition that is accelerated by accumulation of unfolded/misfolded proteins after endoplasmic reticulum environment disturbance, triggered by a variety of physiological and pathological factors, such as nutrient deprivation, altered glycosylation, calcium depletion, oxidative stress, DNA damage and energy disturbance, etc. ERS may initiate the unfolded protein response (UPR) to restore cellular homeostasis or lead to apoptosis. Numerous studies have clarified the link between ERS and cardiovascular diseases. This review focuses on ERS-associated molecular mechanisms that participate in physiological and pathophysiological processes of heart and blood vessels. In addition, a number of drugs that regulate ERS was introduced, which may be used to treat cardiovascular diseases. This review may open new avenues for studying the pathogenesis of cardiovascular diseases and discovering novel drugs targeting ERS.

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Berberine protects human renal proximal tubular cells from hypoxia/reoxygenation injury via inhibiting endoplasmic reticulum and mitochondrial stress pathways

Cited by 98 publications

References 37 publications

Endoplasmic reticulum stress and its effects on renal tubular cells apoptosis in ischemic acute kidney injury

Endoplasmic reticulum stress and its effects on renal tubular cells apoptosis in ischemic acute kidney injury

Ameliorative effect of berberine against gentamicin-induced nephrotoxicity in rats via attenuation of oxidative stress, inflammation, apoptosis and mitochondrial dysfunction

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

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