Lycopene inhibits regulator of calcineurin 1‐mediated apoptosis by reducing oxidative stress and down‐regulating Nucling in neuronal cells

Lim, Sei-Young; Hwang, Sinwoo; Ji, Yu; Lim, Joo Weon; Kim, Hye Young

doi:10.1002/mnfr.201600530

Cited by 24 publications

(13 citation statements)

References 58 publications

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“…The TUNEL assay results indicated that lycopene and insulin individually and simultaneously prevented apoptosis. In support of this result, Lim et al (33) reported that lycopene inhibited apoptosis in neural cells via reducing oxidative stress. They also concluded that the consumption of lycopene-rich foods may prevent neuronal damage induced by oxidative stress in certain neuropathological conditions including Alzheimer's disease.…”

Section: Discussionmentioning

confidence: 74%

Antioxidant and neuroprotective effects of lycopene and insulin in the hippocampus of streptozotocin‑induced diabetic rats

et al. 2018

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In the present study the antioxidant and neuroprotective effects of insulin and lycopene on passive avoidance memory, total antioxidant capacity (TAC), malondialdehyde activity (MDA) and prevention of apoptosis in the hippocampus streptozotocin-induced diabetic rats were examined. The rats were randomly divided to six experimental groups (n=8 per group): Non-diabetic (controls); diabetic; diabetic treated with lycopene; diabetic treated with insulin; diabetic treated with lycopene and insulin; and normal treated with lycopene. Intraperitoneal injection of single dose (60 mg/kg) streptozotocin (STZ) was used to induce the diabetes rat model. The shuttle box test was used for learning and memory assessment. Rats were then sacrificed and hippocampi tissue isolated from the two hemispheres to determine TAC and MDA. Apoptosis rate was also evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling and acridine orange staining assays. The results indicated that lycopene and insulin, solely or in combination, prevented hippocampal neuronal cell death and improved learning and cognition by increasing TAC and decreasing MDA. Collectively, the findings presented herein suggest that insulin and lycopene co-treatment has neuroprotective effect, and ameliorates STZ-induced learning and memory impairment and apoptotic cell death in the hippocampal regions of diabetic rats.

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Section: Discussionmentioning

confidence: 74%

Antioxidant and neuroprotective effects of lycopene and insulin in the hippocampus of streptozotocin‑induced diabetic rats

et al. 2018

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“…In addition, its antioxidant mechanisms are also associated with the elimination of other free radicals, leading to the reduction of intracellular and extracellular ROS levels, and decrease the formation of MDA in plasma and tissue and increase GSH levels and hepatic GSH-Px, SOD, and CAT activities [50]. Also, lycopene also inhibits NF- κ B activation, DNA fragmentation, caspase-3 activation, and cytochrome c release [51].…”

Section: Discussionmentioning

confidence: 99%

Antioxidants as Adjuvants in Periodontitis Treatment: A Systematic Review and Meta-Analysis

Castro

Duarte

Nascimento

et al. 2019

Oxidative Medicine and Cellular Longevity

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This systematic review with meta-analysis aimed to evaluate the effect of antioxidants as an adjuvant in periodontitis treatment. The following databases were consulted: PubMed, Scopus, Web of Science, Cochrane, Lilacs, OpenGrey, and Google Scholar. Based on the PICO strategy, the inclusion criteria comprised interventional studies including periodontitis patients (participants) treated with conventional therapy and antioxidants (intervention) compared to patients treated only with conventional therapy (control) where the periodontal response (outcome) was evaluated. The risk of bias was evaluated using the Cochrane RoB tool (for randomized studies) and ROBINS-I tool (for nonrandomized studies). Quantitative data were analyzed in five random effects meta-analyses considering the following periodontal parameters: clinical attachment loss (CAL), plaque index (PI), gingival index (GI), bleeding on probing (BOP), and probing depth (PD). After all, the level of certainty was measured with the Grading of Recommendation, Assessment, Development, and Evaluation (GRADE) tool. Among the 1884 studies identified, only 15 interventional studies were according to the eligibility criteria and they were included in our review. From them, 4 articles presented a high risk of bias. The meta-analysis showed a statistically significant difference for CAL (SMD 0.29 (0.04, 0.55), p=0.03, I2=13%), PI (SMD 0.41 (0.18, 0.64), p=0.0005, I2=47%), and BOP (SMD 0.55 (0.27, 0.83), p=0.0001, I2=0%). The GRADE tool showed a moderate to high certainty in the quality of evidence depending on the clinical parameter and antioxidants used. These results suggest that the use of antioxidants is an adjunct approach to nonsurgical periodontal therapy which may be helpful in controlling the periodontal status.

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“…Especially, increase in mitochondrial ROS is an important index of mitochondrial dysfunction in neuronal diseases [ 42 , 43 ]. Recently, we showed that lycopene inhibits apoptosis by reducing oxidative stress and downregulating Nucling in neuronal cells transfected with regulator of calcineurin [ 44 ]. In the present study, lycopene significantly inhibited amyloid-β-induced mitochondrial dysfunction, which was proven by its protective effect in reducing both MMP and OCR.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effect of Lycopene on Amyloid-β-Induced Apoptosis in Neuronal Cells

2017

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Alzheimer′s disease (AD) is a fatal neurodegenerative disease. Brain amyloid-β deposition is a crucial feature of AD, causing neuronal cell death by inducing oxidative damage. Reactive oxygen species (ROS) activate NF-κB, which induces expression of Nucling. Nucling is a pro-apoptotic factor recruiting the apoptosome complex. Lycopene is an antioxidant protecting from oxidative stress-induced cell damage. We investigated whether lycopene inhibits amyloid-β-stimulated apoptosis through reducing ROS and inhibiting mitochondrial dysfunction and NF-κB-mediated Nucling expression in neuronal SH-SY5Y cells. We prepared cells transfected with siRNA for Nucling or nontargeting control siRNA to determine the role of Nucling in amyloid-β-induced apoptosis. The amyloid-β increased intracellular and mitochondrial ROS levels, apoptotic indices (p53, Bax/Bcl-2 ratio, caspase-3 cleavage), NF-kB activation and Nucling expression, while cell viability, mitochondrial membrane potential, and oxygen consumption rate decreased in SH-SY5Y cells. Lycopene inhibited these amyloid-β-induced alterations. However, amyloid-β did not induce apoptosis, determined by cell viability and apoptotic indices (p53, Bax/Bcl-2 ratio, caspase-3 cleavage), in the cells transfected with siRNA for Nucling. Lycopene inhibited apoptosis by reducing ROS, and by inhibiting mitochondrial dysfunction and NF-κB-target gene Nucling expression in neuronal cells. Lycopene may be beneficial for preventing oxidative stress-mediated neuronal death in patients with neurodegeneration.

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Lycopene inhibits regulator of calcineurin 1‐mediated apoptosis by reducing oxidative stress and down‐regulating Nucling in neuronal cells

Cited by 24 publications

References 58 publications

Antioxidant and neuroprotective effects of lycopene and insulin in the hippocampus of streptozotocin‑induced diabetic rats

Antioxidant and neuroprotective effects of lycopene and insulin in the hippocampus of streptozotocin‑induced diabetic rats

Antioxidants as Adjuvants in Periodontitis Treatment: A Systematic Review and Meta-Analysis

Inhibitory Effect of Lycopene on Amyloid-β-Induced Apoptosis in Neuronal Cells

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