Geniposide prevents H<sub>2</sub>
O<sub>2</sub>
-induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway

Lu, Wenjing; Kong, Ying; Zhang, W.; Ma, Wenxue; Li, W.; Wang, K.

doi:10.1111/ced.13409

Cited by 33 publications

(21 citation statements)

References 23 publications

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“…An imbalance in the oxidant (non-enzymatic and enzymatic, MPO and NAdH oxidase)/anti-oxidant mechanisms (GSH, Vitamins, Gpx, Prdx, SOd and PON) induces excess ROS production, leading to a state of atherogenic plaque formation (48). Geniposide exerts beneficial activities in human diseases by inhibiting oxidative stress injury (49)(50)(51). Geniposide decreases intracellular ROS accumulation and enhances the antioxidant enzymatic SOd and cAT activities in H 2 O 2 -treated melanocytes (49).…”

Section: Discussionmentioning

confidence: 99%

“…Geniposide exerts beneficial activities in human diseases by inhibiting oxidative stress injury (49)(50)(51). Geniposide decreases intracellular ROS accumulation and enhances the antioxidant enzymatic SOd and cAT activities in H 2 O 2 -treated melanocytes (49). Geniposide also enhances mitochondrial function via attenuating oxidative stress and MdA, and enhancing the antioxidant defense system, resulting in the inhibition of cardiomyocyte apoptosis and protection against hypoxia/reoxygenation injury (14).…”

Section: Discussionmentioning

confidence: 99%

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miR‑21/PTEN pathway mediates the cardioprotection of geniposide against oxidized low‑density�lipoprotein‑induced endothelial injury via suppressing oxidative stress and inflammatory response

et al. 2020

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Oxidized low-density lipoprotein (ox-LdL)-induced vascular endothelial damage, oxidative stress and inflammation play a vital role in the pathophysiology of atherosclerosis. Geniposide is the primary active ingredient from Gardenia jasminoides Ellis associated with anti-oxidative properties and cardioprotective action. However, the therapeutic mechanism of geniposide in atherosclerosis remains unclear. Hence, the present study aimed to elucidate the underlying mechanisms of geniposide in oxidative stress and inflammatory response during ox-LdL injury in human umbilical vein endothelial cells (HUVEcs), focusing particularly on the microRNA (miR)-21/PTEN pathway. The results demonstrated that geniposide pretreatment significantly increased cell viability, decreased lactate dehydrogenase release, increased miR-21 level and decreased PTEN expression under ox-LdL condition. Subsequently, transfection with miR-21 mimic enhanced the protection of geniposide on ox-LdL-induced cytotoxicity and apoptosis (mediated by the upregulation of apoptotic rate and caspase-3 activity), whereas miR-21 inhibitor reversed these effects of geniposide. In addition, geniposide resulted in an anti-oxidant effect as evidenced by the decrease in reactive oxygen species generation, malondialdehyde content and NAdPH oxidase 2 expression, and the increase in superoxide dismutase, glutathione peroxidase and catalase activities in ox-LdL-treated HUVEcs, which were exacerbated by miR-21 mimic and reversed by miR-21 inhibitor. Furthermore, geniposide mitigated the ox-LdL-induced inflammatory response, demonstrated by a downregulation of pro-inflammatory cytokine (IL-1β, IL-6, and TNF-α) levels and an upregulation of anti-inflammatory cytokine (IL-10) level. However, miR-21 mimic enhanced, whereas miR-21 inhibitor attenuated, these effects of geniposide. In conclusion, the present results indicated that geniposide protects HUVEcs from ox-LdL injury by inhibiting oxidative stress and inflammation, and that these effects are partly due to the enhancement of the miR-21/PTEN pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

miR‑21/PTEN pathway mediates the cardioprotection of geniposide against oxidized low‑density�lipoprotein‑induced endothelial injury via suppressing oxidative stress and inflammatory response

et al. 2020

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“…Geniposide is an active ingredient of traditional Chinese herbal medicine Gardenia jasminoides Ellis, which is extensively applied in clinic to treat stroke in China. Geniposide has various pharmacological properties, such as anti-inflammatory, antidiabetic, anti-fibrotic, antioxidative, anti-apoptotic and antitumour activities [5][6][7][8][9]. Besides this, geniposide was revealed to be beneficial in suppressing Helicobacter pylori infections [10].…”

Section: Introductionmentioning

confidence: 99%

Geniposide protects PC12 cells from lipopolysaccharide-evoked inflammatory injury via up-regulation of miR-145-5p

Zhang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Geniposide is an active ingredient with anti-apoptotic and anti-inflammatory properties. This study was to examine the effects of geniposide on a cell model of spinal cord injury (SCI). PC12 cells were administrated with geniposide before subjected to LPS. The effects of geniposide were analyzed by utilizing CCK-8 assay, apoptosis assay, ELISA, RT-qPCR and Western blot. We found that PC12 cells viability was unchanged by treating with geniposide. However, geniposide with concentrations of 200 or 300 lg/mL significantly mitigated LPS-evoked viability loss. Meanwhile, apoptosis driven by LPS was mitigated by geniposide, which accompanied with p53, Bax and cleaved caspase-3 down-regulation, and Bcl-2 up-regulation. Besides this, the expression and release of IL-1b, IL-6, IL-8 and TNF-a evoked by LPS were mitigated by geniposide. miR-145-5p was a target of geniposide. miR-145-5p expression was up-regulated by geniposide, and geniposide did not protect PC12 cells against LPS injury when miR-145-5p was silenced. Moreover, geniposide inhibited NF-jB and JNK pathways via up-regulating miR-145-5p. In short, the present work described the neuroprotective effects of geniposide by targeting miR-145-5p. Further mechanisms involved in geniposide's beneficial effects are correlated with the inhibited NF-jB and JNK pathways. HIGHLIGHTS 1. Geniposide prevents LPS-induced injury in PC12 cells; 2. Geniposide up-regulates miR-145-5p; 3. Geniposide protects PC12 cells via up-regulation of miR-145-5p; 4. Geniposide inhibits NF-jB and JNK pathways via up-regulation of miR-145-5p.

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“…For vitiligo in vitro cell model conduction, normal human melanocytes were treated with 250 lmol/L H 2 O 2 (Sigma-Aldrich, St. Louis, MO, USA) for 4 h to induce oxidative stress [26].…”

Section: Vitiligo In Vitro Cell Model Conductionmentioning

confidence: 99%

MiR-217 inhibition relieves oxidative stress-induced melanocyte damage by targeting sirtuin 1

Huang

Sun

2020

Biotechnology & Biotechnological Equipment

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Vitiligo is caused by the disappearance of melanocyte function in the skin, but the mechanism has not been fully elucidated. This study aimed to investigate the expression and role of miR-217 in dysfunctional human primary melanocytes caused by oxidative stress, so as to explore its potential role in vitiligo. Hydrogen peroxide (H 2 O 2 ) was used to induce the oxidative damage of melanocytes. The levels of sirtuin 1 (SIRT1) and miR-217 were measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and or Western blot assay. TargetScan and dual luciferase reporter gene assay were used to confirm the relationship between SIRT1 and miR-217. Cell viability and cell apoptosis were analysed by 3-(4,5-dimethyl-2-thiazolyl)À2,5diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry assay, respectively. Reactive oxygen species (ROS) production, superoxide dismutase (SOD) and catalase (CAT) activities were determined using specific assay kits. SIRT1 was down-regulated, while miR-217 was up-regulated in H 2 O 2 -induced human primary melanocytes. SIRT1 was a target gene of miR-217. Inhibition of miR-217 increased cell viability and inhibited cell apoptosis in H 2 O 2 -treated melanocytes. Besides, inhibition of miR-217 enhanced the antioxidant activity of SOD and CAT and reduced the accumulation of intracellular ROS. Notably, all these effects were reversed by SIRT1-siRNA. The data indicated that SIRT1 was down-regulated, while miR-217 was up-regulated in dysfunctional human primary melanocytes caused by oxidative stress, and miR-217 inhibition relieved oxidative stress-induced melanocyte damage via targeting SIRT1, indicating that miR-217 might a potential target for vitiligo treatment. ARTICLE HISTORY

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Geniposide prevents H₂ O₂ -induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway

Abstract: Based on these results, geniposide protects human melanocytes from H O -induced oxidative damage, and the PI3K-Akt signalling pathway is involved in its antioxidant effect.

Cited by 33 publications

References 23 publications

miR‑21/PTEN pathway mediates the cardioprotection of geniposide against oxidized low‑density�lipoprotein‑induced endothelial injury via suppressing oxidative stress and inflammatory response

miR‑21/PTEN pathway mediates the cardioprotection of geniposide against oxidized low‑density�lipoprotein‑induced endothelial injury via suppressing oxidative stress and inflammatory response

Geniposide protects PC12 cells from lipopolysaccharide-evoked inflammatory injury via up-regulation of miR-145-5p

MiR-217 inhibition relieves oxidative stress-induced melanocyte damage by targeting sirtuin 1

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Geniposide prevents H2 O2 -induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway

Abstract: Based on these results, geniposide protects human melanocytes from H O -induced oxidative damage, and the PI3K-Akt signalling pathway is involved in its antioxidant effect.

Cited by 33 publications

References 23 publications

miR‑21/PTEN pathway mediates the cardioprotection of geniposide against oxidized low‑density�lipoprotein‑induced endothelial injury via suppressing oxidative stress and inflammatory response

miR‑21/PTEN pathway mediates the cardioprotection of geniposide against oxidized low‑density�lipoprotein‑induced endothelial injury via suppressing oxidative stress and inflammatory response

Geniposide protects PC12 cells from lipopolysaccharide-evoked inflammatory injury via up-regulation of miR-145-5p

MiR-217 inhibition relieves oxidative stress-induced melanocyte damage by targeting sirtuin 1

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Geniposide prevents H₂ O₂ -induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway