Protective effect of tomatine against hydrogen peroxide-induced neurotoxicity in neuroblastoma (SH-SY5Y) cells

Huang, Shao-lan; He, Hui; Zou, Kun; Bai, Cai-hong; Xue, Yanhong; Wang, Junzhi; Chen, Jianfeng

doi:10.1111/jphp.12205

Cited by 25 publications

(12 citation statements)

References 39 publications

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“…BDNF regulates the synthesis of synaptic proteins and elevates synaptic efficacy, necessary precursors for appropriate neuronal function, survival, and apoptosis [ 22 ]. Impaired regulation of BDNF expression has been implicated in mood and anxiety disorders [ 34 ] and in cognitive and neurodegenerative diseases [ 35 ]; environment stimuli such as H 2 O 2 reduced BDNF expression levels in SH-SY5Y cells [ 36 ]. As expected, in our study, BDNF mRNA and protein levels significantly decreased in a dose-dependent manner after a 48-hour exposure to various concentrations of PFOS.…”

Section: Discussionmentioning

confidence: 99%

PFOS Disturbs BDNF-ERK-CREB Signalling in Association with Increased MicroRNA-22 in SH-SY5Y Cells

He²,

Cui-zhen

et al. 2015

BioMed Research International

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Perfluorooctane sulfonate (PFOS), a ubiquitous environmental pollutant, is neurotoxic to mammalian species. However, the underlying mechanism of its neurotoxicity was unclear. We hypothesized that PFOS suppresses BDNF expression to produce its neurotoxic effects by inhibiting the ERK-CREB pathway. SH-SY5Y human neuroblastoma cells were exposed to various concentrations of PFOS to examine the role of the BDNF-ERK-CREB signalling pathway in PFOS-induced apoptosis and cytotoxicity. Furthermore, to ascertain the mechanism by which PFOS reduces BDNF signalling, we examined the expression levels of miR-16 and miR-22, which potentially regulate BDNF mRNA translation at the posttranscriptional level. Results indicated that PFOS significantly decreased cell viability and induced apoptosis in SH-SY5Y cells. In addition, BDNF and pERK protein levels decreased after PFOS treatment; however, pCREB protein levels were significantly elevated in PFOS treated groups. TrkB protein expression increased in the 10 μM and 50 μM PFOS groups and significantly decreased in the 100 μM PFOS group. Our results demonstrated that PFOS exposure decreased miR-16 expression and increased miR-22 expression, which may represent a possible mechanism by which PFOS decreases BDNF protein levels. PFOS may inhibit BDNF-ERK-CREB signalling by increasing miR-22 levels, which may, in part, explain the mechanism of PFOS neurotoxicity.

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Section: Discussionmentioning

confidence: 99%

PFOS Disturbs BDNF-ERK-CREB Signalling in Association with Increased MicroRNA-22 in SH-SY5Y Cells

He²,

Cui-zhen

et al. 2015

BioMed Research International

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“…Tomatine ( 168) was illustrated to exert significant neuroprotective effect on H 2 O 2 -induced SH-SY5Y cells, by enhancing intracellular anti-oxidant enzyme activity and brain-derived neurotrophic factor expression and restraining H 2 O 2 -induced oxidative stress [106]. Isojuripidine ( 190 ) displayed spasmolytic activity by hindering phasic contractions induced by both histamine and acetylcholinein guinea-pig ileum [69].…”

Section: Chemical Constituents and Their Biological Propertiesmentioning

confidence: 99%

“…Various bioactivities e.g. antibacterial [80, 384, 403, 406, 407], anticancer [13, 305, 458], antidiabetic [182, 183], antifungal [279], anti-inflammatory [303], CNS depressant [294], leishmanicidal [182, 183], molluscicidal [384, 403, 406, 407], neurotoxicity [106], schistosomicidal [185, 186, 447, 457], spasmolytic [70] and trypanocidal [185, 186, 447, 457] were highlighted as have been exhibited by steroidal alkaloids of Solanum .…”

Section: Chemical Constituents and Their Biological Propertiesmentioning

confidence: 99%

The Genus Solanum: An Ethnopharmacological, Phytochemical and Biological Properties Review

Kaunda

Zhang

2019

Nat. Prod. Bioprospect.

103

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Over the past 30 years, the genus Solanum has received considerable attention in chemical and biological studies. Solanum is the largest genus in the family Solanaceae, comprising of about 2000 species distributed in the subtropical and tropical regions of Africa, Australia, and parts of Asia, e.g., China, India and Japan. Many of them are economically significant species. Previous phytochemical investigations on Solanum species led to the identification of steroidal saponins, steroidal alkaloids, terpenes, flavonoids, lignans, sterols, phenolic comopunds, coumarins, amongst other compounds. Many species belonging to this genus present huge range of pharmacological activities such as cytotoxicity to different tumors as breast cancer (4T1 and EMT), colorectal cancer (HCT116, HT29, and SW480), and prostate cancer (DU145) cell lines. The biological activities have been attributed to a number of steroidal saponins, steroidal alkaloids and phenols. This review features 65 phytochemically studied species of Solanum between 1990 and 2018, fetched from SciFinder, Pubmed, ScienceDirect, Wikipedia and Baidu, using “Solanum” and the species’ names as search terms (“all fields”).

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“…The development of effective therapeutics against cerebral ischemia has been challenging worldwide. As a novel therapeutic candidate, tomatidine is able to cross the blood-brain barrier is identified with neuroprotection from ischemic injury in the context of neurodegenerative disorders such as Alzheimer's disease [22,23]. Studies using varying tissues and/or organs provide mounting evidences and indicate that tomatidine-induced cytoprotection against ischemic injuries was associated with antioxidant, anti-inflammatory and anti-cancer activities [16,17,22].…”

Section: Discussionmentioning

confidence: 99%

Tomatidine provides mitophagy‐independent neuroprotection after ischemic injury

et al. 2021

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Cerebral ischemia is one of the leading causes of human mortality and disability worldwide. The treatment of cerebral ischemia is refractory due to its short therapeutic window and lack of effective clinical drugs.Mitophagy, the autophagic elimination of damaged mitochondria, attenuates neuronal injury in cerebral ischemia, indicating the potential of mitophagy inducers as therapies for cerebral ischemia. We previously determined that, by enhancing autophagy flux, the steroidal alkaloid tomatidine can function as a neuroprotective agent against ischemic injury. However, its effects on mitophagy remain unknown. For this purpose, neuroblastoma cell lines Neuro-2a (N2a) and SH-SY5Y were subjected to ischemic injury induced by oxygen-glucose deprivation/reperfusion (OGD/R), then treated with tomatidine. OGD/R induced a general decrease of cellular contents, and the present study revealed that tomatidine had no impact on mitophagy. In addition, tomatidine did not affect mitochondrial contents, including translocase of outer mitochondrial membrane 20 (TOM20) and voltage-dependent anion channel 1 (VDAC1), in either OGD/R-treated or intact SH-SY5H cells. Our results indicate that tomatidine exhibits its neuroprotective effects by enhancing autophagy but potentially mitophagy-independent manner, and provide insights for further investigation into its mechanism(s) and potential therapeutic use against cerebral ischemia.

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Protective effect of tomatine against hydrogen peroxide-induced neurotoxicity in neuroblastoma (SH-SY5Y) cells

Cited by 25 publications

References 39 publications

PFOS Disturbs BDNF-ERK-CREB Signalling in Association with Increased MicroRNA-22 in SH-SY5Y Cells

PFOS Disturbs BDNF-ERK-CREB Signalling in Association with Increased MicroRNA-22 in SH-SY5Y Cells

The Genus Solanum: An Ethnopharmacological, Phytochemical and Biological Properties Review

Tomatidine provides mitophagy‐independent neuroprotection after ischemic injury

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