Berberine exerts nephroprotective effect against cisplatin-induced kidney damage through inhibition of oxidative/nitrosative stress, inflammation, autophagy and apoptosis

Domitrović, Robert; Cvijanović, Olga; Pugel, Ester Pernjak; Škoda, Marko; Mikelić, Lorena; Crnčević-Orlić, Željka

doi:10.1016/j.fct.2013.09.003

Cited by 155 publications

(91 citation statements)

References 57 publications

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“…The berberine analogue, 8,8-dimethyldihydroberberine, improved glucose tolerance and alleviates insulin resistance in db/db mice (Cheng et al, 2010). Most recently, berberine exerted nephroprotective and neuroprotective effects through inhibiting oxidative stress (Domitrovic et al, 2013;Moghaddam et al, 2014). Consistent with these earlier reports, the present study showed that in vitro berberine treatment restored insulin secretion through inhibiting HG-stimulated oxidative stress as berberine normalized HG-induced elevation in nitrotyrosine level and HG-induced reduction in SOD1 expression in INS-1E cells …”

Section: Discussionsupporting

confidence: 81%

Uncoupling protein‐2 mediates the protective action of berberine against oxidative stress in rat insulinoma INS‐1E cells and in diabetic mouse islets

Liu

Gao

et al. 2014

British J Pharmacology

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Background and PurposeUncoupling protein‐2 (UCP2) may regulate glucose‐stimulated insulin secretion. The current study investigated the effects of berberine, an alkaloid found in many medicinal plants, on oxidative stress and insulin secretion through restoration of UCP2 expression in high glucose (HG)‐treated INS‐1E cells and rat islets or in db/db mouse islets.Experimental ApproachMouse and rat pancreatic islets were isolated. Nitrotyrosine, superoxide dismutase (SOD)‐1 and UCP2 expression and AMPK phosphorylation were examined by Western blotting. Insulin secretion was measured by elisa. Mitochondrial reactive oxygen species (ROS) production was detected by confocal microscopy.Key ResultsIncubation of INS‐1E cells and rat islets with HG (30 mmol·L−1; 8 h) elevated nitrotyrosine level, reduced SOD‐1 and UCP2 expression and AMPK phosphorylation, and inhibited glucose‐stimulated insulin secretion. HG also increased mitochondrial ROS in INS‐1E cells. Co‐treatment with berberine inhibited such effects. The AMPK inhibitor compound C, the UCP2 inhibitor genipin and adenovirus ucp2 shRNA inhibited these protective effects of berberine. Furthermore, compound C normalized berberine‐stimulated UCP2 expression but genipin did not affect AMPK phosphorylation. Islets from db/db mice exhibited elevated nitrotyrosine levels, reduced expression of SOD‐1 and UCP2 and AMPK phosphorylation, and decreased insulin secretion compared with those from db/m+ mice. Berberine also improved these defects in diabetic islets and genipin blocked the effects of berberine.Conclusions and ImplicationsBerberine inhibited oxidative stress and restored insulin secretion in HG‐treated INS‐IE cells and diabetic mouse islets by activating AMPK and UCP2. UCP2 is an important signalling molecule in mediating anti‐diabetic effects of berberine.

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Section: Discussionsupporting

confidence: 81%

Uncoupling protein‐2 mediates the protective action of berberine against oxidative stress in rat insulinoma INS‐1E cells and in diabetic mouse islets

Liu

Gao

et al. 2014

British J Pharmacology

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“…BBR is an isoquinoline alkaloid, the anti-apoptotic property of which has been applied extensively to a variety of diseases [25,32,33]. Attenuating the process of apoptosis [8,34].…”

Section: Discussionmentioning

confidence: 99%

“…1) is a botanical alkaloid derived from several species of medicinal herbs, including Coptis chinensis and Berberis aristate [20]; BBR has shown multiple pharmacological effects, including antibiotic [21], anti-inflammatory [22], anticancer [23], anti-oxidative [24], and anti-apoptotic [25] effects. Recent studies have demonstrated that BBR decreases IL-1b-stimulated glycosaminoglycan release and NO production, and down-regulates matrix metalloproteinases expression in vitro and in vivo [26,27].…”

Section: Introductionmentioning

confidence: 99%

Berberine prevents nitric oxide-induced rat chondrocyte apoptosis and cartilage degeneration in a rat osteoarthritis model via AMPK and p38 MAPK signaling

et al. 2015

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Chondrocyte apoptosis is an important mechanism involved in osteoarthritis (OA). Berberine (BBR), a plant alkaloid derived from Chinese medicine, is characterized by multiple pharmacological effects, such as anti-inflammatory and anti-apoptotic activities. This study aimed to evaluate the chondroprotective effect and underlying mechanisms of BBR on sodium nitroprusside (SNP)-stimulated chondrocyte apoptosis and surgically-induced rat OA model. The in vitro results revealed that BBR suppressed SNP-stimulated chondrocyte apoptosis as well as cytoskeletal remodeling, down-regulated expressions of inducible nitric oxide synthase (iNOS) and caspase-3, and up-regulated Bcl-2/Bax ratio and Type II collagen (Col II) at protein levels, which were accompanied by increased adenosine monophosphate-activated protein kinase (AMPK) phosphorylation and decreased phosphorylation of p38 mitogen-activated protein kinase (MAPK). Furthermore, the anti-apoptotic effect of BBR was blocked by AMPK inhibitor Compound C (CC) and adenosine-9-β-D-arabino-furanoside (Ara A), and enhanced by p38 MAPK inhibitor SB203580. In vivo experiment suggested that BBR ameliorated cartilage degeneration and exhibited an anti-apoptotic effect on articular cartilage in a rat OA model, as demonstrated by histological analyses, TUNEL assay and immunohistochemical analyses of caspase-3, Bcl-2 and Bax expressions. These findings suggest that BBR suppresses SNP-stimulated chondrocyte apoptosis and ameliorates cartilage degeneration via activating AMPK signaling and suppressing p38 MAPK activity.

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“…Mitochondria may involve at early stage compared to other nonmitochondrial enzymatic ROS generation (Mukhopadhyay et al, 2011). Nitric oxide is produced from iNOS followed by in situ production of cell killing peroxynitrite radical (Domitrovic et al, 2013;Pan et al, 2014). Protein adducts with 3-nitrotyrosine (also known as protein nitration) is the footprint of peroxynitrite formation and the protein nitration was reduced by acetovanillone treatment in cisplatin treated mice.…”

Section: Acetovanillone and Cisplatin Synergistically Effect Cell Deamentioning

confidence: 99%

Pharmacological inhibition of NADPH oxidase protects against cisplatin induced nephrotoxicity in mice by two step mechanism

Wang

Luo²,

Pān

et al. 2015

Food and Chemical Toxicology

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Berberine exerts nephroprotective effect against cisplatin-induced kidney damage through inhibition of oxidative/nitrosative stress, inflammation, autophagy and apoptosis

Cited by 155 publications

References 57 publications

Uncoupling protein‐2 mediates the protective action of berberine against oxidative stress in rat insulinoma INS‐1E cells and in diabetic mouse islets

Uncoupling protein‐2 mediates the protective action of berberine against oxidative stress in rat insulinoma INS‐1E cells and in diabetic mouse islets

Berberine prevents nitric oxide-induced rat chondrocyte apoptosis and cartilage degeneration in a rat osteoarthritis model via AMPK and p38 MAPK signaling

Pharmacological inhibition of NADPH oxidase protects against cisplatin induced nephrotoxicity in mice by two step mechanism

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