Curcumin alleviates arsenic-induced toxicity in PC12 cells via modulating autophagy/apoptosis

Rahaman, Md. Shiblur; Banik, Subrata; Akter, Mahmuda; Rahman, Mostafizur; Hosokawa, Toshiyuki; Saito, Takeshi; Kurasaki, Masaaki

doi:10.1016/j.ecoenv.2020.110756

Cited by 47 publications

(25 citation statements)

References 54 publications

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“…In keeping with this, the present study shows that CUR protects against METH intoxication concomitantly with suppressing α-synuclein accumulation, polymerization likely due to autophagy activation. The ability of CUR to produce neuroprotection may also rely on additional properties of the compound such as the powerful anti-oxidant activity and free radical scavenging properties [ 42 , 43 , 44 , 45 , 46 , 47 , 48 ]. However, the autophagy activation per se seems to provide full protection, thus leaving addition mechanisms non-necessary.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Curcumin in Methamphetamine-Induced Toxicity

et al. 2021

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Curcumin (CUR), a natural polyphenol extracted from rhizome of the Curcuma longa L, has received great attention for its multiple potential health benefits as well as disease prevention. For instance, CUR protects against toxic agents acting on the human body, including the nervous system. In detail, CUR possesses, among others, strong effects as an autophagy activator. The present study indicates that CUR counteracts methamphetamine (METH) toxicity. Such a drug of abuse is toxic by disturbing the autophagy machinery. We profited from an unbiased, low variable cell context by using rat pheochromocytoma PC12 cell line. In such a system, a strong protection was exerted by CUR against METH toxicity. This was associated with increased autophagy flux, merging of autophagosomes with lysosomes and replenishment of autophagy vacuoles with LC3, which instead is moved out from the vacuoles by METH. This is expected to enable the autophagy machinery. In fact, while in METH-treated cells the autophagy substrates α-synuclein accumulates in the cytosol, CUR speeds up α-synuclein clearance. Under the effects of CUR LC3 penetrate in autophagy vacuoles to commit them to cell clearance and promotes the autophagy flux. The present data provide evidence that CUR counteracts the neurotoxic effects induced by METH by promoting autophagy.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Curcumin in Methamphetamine-Induced Toxicity

et al. 2021

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“…On the other hand, it was observed that RUT showed an anti-autophagic effect and decreased beclin-1, LC3A and LC3B levels. Previous studies have reported that naturally occurring antioxidants reduce autophagy, which is increased by different toxic compounds [58,59].…”

Section: Discussionmentioning

confidence: 97%

Rutin Protects from Destruction by Interrupting the Pathways Playing a Role in the Possible Damage Mechanism of Sodium Valproate in the Liver and Kidney Tissues of Rats

Kandemir

İleritürk

Gür

2021

Preprint

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Background: The present study investigated the effects of rutin (RUT), which has various biological and pharmacological properties, on liver and kidney damage caused by histone deacetylase inhibitor valproic acid (VLP), which is used in the treatment of many psychiatric disorders.Methods and Results: In the study, 50 or 100 mg/kg RUT treatment was administered 30 minutes after 500 mg/kg VLP was given to rats for 14 days. Then, some pathways that may be involved in the damage mechanism of VLP in liver and kidney tissues were investigated using biochemical, RT-PCR and Western blotting techniques. The results show that the levels of MDA induced by VLP in liver and kidney tissues decreased after RUT treatment, and the levels of SOD, CAT, GPx and GSH suppressed by VLP increased after RUT administration. It was observed that ER stress induced by oxidative stress was alleviated by suppressing the expressions of ATF-6, PERK, IRE1 and GRP78 after RUT treatment. It was observed that the expressions of NF-kB, TNF-a, IL-6, JAK2 and STAT3 in the inflammatory pathway increased after VLP administration, while RUT treatment decreased the levels of these markers. It is also among the data obtained that the levels of markers that play a role in the regulation of apoptosis (Bax, Bcl-2, kaspaz-3, pERK, pJNK) or autophagy (Beclin-1, LC3A, LC3B) approach the control group after RUT treatment.Conclusions: Taken together, it was determined that RUT treatment protected against liver and kidney damage by attenuating VLP-induced oxidative stress, ER stress, inflammation, apoptosis and autophagy.

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“…As 3+ induces apoptosis and autophagy in PC12 cells through the downregulation of mTOR and Akt and upregulation of ULK1 and LC3 II. However, this effect is reversed following pretreatment with curcumin (Rahaman et al, 2020). ULK1 is a serine/threonine-specific protein kinase that plays an important role in the initiation of autophagy (C. Wang et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Hydrogen sulfide alleviates apoptosis and autophagy induced by beryllium sulfate in 16HBE cells

Liu

Yuan

et al. 2021

J of Applied Toxicology

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Beryllium and its compounds are systemic toxicants that are widely applied in many industries. Hydrogen sulfide has been found to protect cells. The present study aimed to determine the protective mechanisms involved in hydrogen sulfide treatment of 16HBE cells following beryllium sulfate-induced injury. 16HBE cells were treated with beryllium sulfate doses ranging between 0 and 300 μM BeSO 4 .Additionally, 16HBE cells were subjected to pretreatment with either a 300 μM dose of sodium hydrosulfide (a hydrogen sulfide donor) or 10 mM DLpropargylglycine (a cystathionine-γ-lyase inhibitor) for 6 hr before then being treated with 150 μM beryllium sulfate for 48 hr. This study illustrates that beryllium sulfate induces a reduction in cell viability, increases lactate dehydrogenase (LDH) release, and increases cellular apoptosis and autophagy in 16HBE cells.Interestingly, pretreating 16HBE cells with sodium hydrosulfide significantly reduced the beryllium sulfate-induced apoptosis and autophagy. Moreover, it increased the mitochondrial membrane potential and alleviated the G2/M-phase cell cycle arrest. However, pretreatment with 10 mM DL-propargylglycine promoted the opposite effects. PI3K/Akt/mTOR and Nrf2/ARE signaling pathways are also activated following pretreatment with sodium hydrosulfide. These results indicate the protection provided by hydrogen sulfide in 16HBE cells against beryllium sulfate-induced injury is associated with the inhibition of apoptosis and autophagy through the activation of the PI3K/Akt/mTOR and Nrf2/ARE signaling pathways. Therefore, hydrogen sulfide has the potential to be a promising candidate in the treatment against beryllium disease.

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Curcumin alleviates arsenic-induced toxicity in PC12 cells via modulating autophagy/apoptosis

Cited by 47 publications

References 54 publications

Neuroprotective Effects of Curcumin in Methamphetamine-Induced Toxicity

Neuroprotective Effects of Curcumin in Methamphetamine-Induced Toxicity

Rutin Protects from Destruction by Interrupting the Pathways Playing a Role in the Possible Damage Mechanism of Sodium Valproate in the Liver and Kidney Tissues of Rats

Hydrogen sulfide alleviates apoptosis and autophagy induced by beryllium sulfate in 16HBE cells

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