Curcumin Inhibits Cell Damage and Apoptosis Caused by Thapsigargin-Induced Endoplasmic Reticulum Stress Involving the Recovery of Mitochondrial Function Mediated by Mitofusin-2

Zhou, He-Yan; Sun, Yuanyuan; Chang, Peng; Huang, Han-Chang

doi:10.1007/s12640-022-00481-y

Cited by 12 publications

(11 citation statements)

References 40 publications

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Section: Discussionmentioning

confidence: 99%

“…10 The application of curcumin prior to UVB exposure prevents CPD expression and cell damage as well as play a role in accelerating CPD repair by influencing cellular processes such as cycle cell, differentiation and DNA repairment through the mutS homolog 2 (MSH2) enzyme. 10,20 Furthermore, an in vitro study on squamous cell carcinoma cell lines showed that curcumin decreases UV-induced apoptosis and inflammation through inhibition of nuclear factor-κB (NF-κB). 20,21 In contrast with CPD, the effect of curcumin against 8-OHdG, one of the key markers for cellular oxidative stress, following single UVB exposure showed strong protective effect.…”

Section: Discussionmentioning

confidence: 99%

“…10,20 Furthermore, an in vitro study on squamous cell carcinoma cell lines showed that curcumin decreases UV-induced apoptosis and inflammation through inhibition of nuclear factor-κB (NF-κB). 20,21 In contrast with CPD, the effect of curcumin against 8-OHdG, one of the key markers for cellular oxidative stress, following single UVB exposure showed strong protective effect. The best protective effect was shown by 10μM concentration.…”

Section: Discussionmentioning

confidence: 99%

“…Subjects used in our study were healthy albino mice aged 7 weeks old that weighed [20][21][22][23][24][25][26][27][28][29][30]…”

Section: Subjectsmentioning

confidence: 99%

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Topical Curcumin as Chemoprotector Against Photoproducts Production: The Role of Cyclobutyl Pyrimidine Dimers, 8-Hydroxy2ʹDeoxyguanosine Expression and Epidermal Hyperplasia in Acute and Chronic UVB-Induced Mice

Djawad¹,

Yusuf²,

Miskad³

et al. 2022

CCID

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Background Ultraviolet B (UVB) exposure leads to formation of photoproducts leading to cellular damage. Prevention using sunscreen can sometimes be inadequate and can be an economic burden. Recent studies have suggested the photoprotective effect of curcumin. Objective To examine the acute and chronic photoprotective effect of topical curcumin, using cyclobutyl pyrimidine dimers (CPD) and 8-hydroxy2ʹdeoxyguanosine (8-OHdG) expression as markers of DNA-induced damage, and epidermal hyperplasia on UVB-induced mice. Methods Three treatment groups were established. Group A (negative control) consisted of 5 mice, Group B and C were further divided into two categories to assess acute and chronic effects of topical curcumin and UVB radiation. Each consisted of six subgroups of five mice. Subgroup 1; UVB exposure only (positive control) subgroup 2; acetone and UVB exposure, subgroup 3–6; topical curcumin application of 100nM, 1µM, 10µM, and 100µM concentrations, respectively. In Group C, there were two categories that received 3x/week UVB exposure for three weeks which effects were being observed at 24 hours and 10 days after the last exposure. The topical curcumin dose was 2mg/mL/cm 2 applied 30 minutes prior to 343mJ/cm 2 /day UVB irradiation. Skin biopsy was done one hour after the last UVB exposure for immunohistochemical and histopathology examinations. Results Topical curcumin showed a limited yet robust protective effect against CPD and 8-OHdG expression in Group B, while in Group C all concentrations showed significant CPD and 8-OHdG inhibition after 10 days of UVB exposure. The 10µM and 100µM concentrations showed the best epidermal hyperplasia inhibition effect (p<0.05). No significant differences were found in terms in efficacy either in single nor daily application. Conclusion Topical curcumin can prevent the formation of the photoproducts CPD and 8-OHdG and epidermal hyperplasia in both acute and chronic exposure in UVB-induced mice.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…Subjects used in our study were healthy albino mice aged 7 weeks old that weighed [20][21][22][23][24][25][26][27][28][29][30]…”

Section: Subjectsmentioning

confidence: 99%

See 2 more Smart Citations

Topical Curcumin as Chemoprotector Against Photoproducts Production: The Role of Cyclobutyl Pyrimidine Dimers, 8-Hydroxy2ʹDeoxyguanosine Expression and Epidermal Hyperplasia in Acute and Chronic UVB-Induced Mice

Djawad¹,

Yusuf²,

Miskad³

et al. 2022

CCID

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“… Xu et al (2018 ) showed that a combination of curcumin and vagus nerve stimulation restored behavioral deficits by inhibiting apoptosis after cerebral ischemia, with the involvement of the Akt/ERK2 pathway. Notably, curcumin inhibits cellular damage and apoptosis by diminishing the endoplasmic reticulum stress (ERS) ( Cheng et al, 2020 ; Keshk et al, 2020 ; Zhou et al, 2022 ). Chhunchha et al (2013 ) reported that curcumin abated hypoxia-induced ERS-mediated cell death in mouse hippocampal cells by enhancing peroxiredoxin 6 (Prdx6) expressions and inhibiting NF-κB activation.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms Underlying Curcumin-Induced Neuroprotection in Cerebral Ischemia

Feng

Meng²

2022

Front. Pharmacol.

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Ischemic stroke is the leading cause of death and disability worldwide, and restoring the blood flow to ischemic brain tissues is currently the main therapeutic strategy. However, reperfusion after brain ischemia leads to excessive reactive oxygen species production, inflammatory cell recruitment, the release of inflammatory mediators, cell death, mitochondrial dysfunction, endoplasmic reticulum stress, and blood–brain barrier damage; these pathological mechanisms will further aggravate brain tissue injury, ultimately affecting the recovery of neurological functions. It has attracted the attention of researchers to develop drugs with multitarget intervention effects for individuals with cerebral ischemia. A large number of studies have established that curcumin plays a significant neuroprotective role in cerebral ischemia via various mechanisms, including antioxidation, anti-inflammation, anti-apoptosis, protection of the blood–brain barrier, and restoration of mitochondrial function and structure, restoring cerebral circulation, reducing infarct volume, improving brain edema, promoting blood–brain barrier repair, and improving the neurological functions. Therefore, summarizing the results from the latest literature and identifying the potential mechanisms of action of curcumin in cerebral ischemia will serve as a basis and guidance for the clinical applications of curcumin in the future.

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Calcium (Ca²⁺) hemostasis, mitochondria, autophagy, and mitophagy contribute to Alzheimer's disease as early moderators

Hadi,

Mortaja,

Hadi

2024

Cell Biochemistry & Function

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This review rigorously investigates the early cerebral changes associated with Alzheimer's disease, which manifest long before clinical symptoms arise. It presents evidence that the dysregulation of calcium (Ca2+) homeostasis, along with mitochondrial dysfunction and aberrant autophagic processes, may drive the disease's progression during its asymptomatic, preclinical stage. Understanding the intricate molecular interplay that unfolds during this critical period offers a window into identifying novel therapeutic targets, thereby advancing the treatment of neurodegenerative disorders. The review delves into both established and emerging insights into the molecular alterations precipitated by the disruption of Ca2+ balance, setting the stage for cognitive decline and neurodegeneration.

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Curcumin Inhibits Cell Damage and Apoptosis Caused by Thapsigargin-Induced Endoplasmic Reticulum Stress Involving the Recovery of Mitochondrial Function Mediated by Mitofusin-2

Cited by 12 publications

References 40 publications

Topical Curcumin as Chemoprotector Against Photoproducts Production: The Role of Cyclobutyl Pyrimidine Dimers, 8-Hydroxy2ʹDeoxyguanosine Expression and Epidermal Hyperplasia in Acute and Chronic UVB-Induced Mice

Topical Curcumin as Chemoprotector Against Photoproducts Production: The Role of Cyclobutyl Pyrimidine Dimers, 8-Hydroxy2ʹDeoxyguanosine Expression and Epidermal Hyperplasia in Acute and Chronic UVB-Induced Mice

Mechanisms Underlying Curcumin-Induced Neuroprotection in Cerebral Ischemia

Calcium (Ca²⁺) hemostasis, mitochondria, autophagy, and mitophagy contribute to Alzheimer's disease as early moderators

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Curcumin Inhibits Cell Damage and Apoptosis Caused by Thapsigargin-Induced Endoplasmic Reticulum Stress Involving the Recovery of Mitochondrial Function Mediated by Mitofusin-2

Cited by 12 publications

References 40 publications

Topical Curcumin as Chemoprotector Against Photoproducts Production: The Role of Cyclobutyl Pyrimidine Dimers, 8-Hydroxy2ʹDeoxyguanosine Expression and Epidermal Hyperplasia in Acute and Chronic UVB-Induced Mice

Topical Curcumin as Chemoprotector Against Photoproducts Production: The Role of Cyclobutyl Pyrimidine Dimers, 8-Hydroxy2ʹDeoxyguanosine Expression and Epidermal Hyperplasia in Acute and Chronic UVB-Induced Mice

Mechanisms Underlying Curcumin-Induced Neuroprotection in Cerebral Ischemia

Calcium (Ca2+) hemostasis, mitochondria, autophagy, and mitophagy contribute to Alzheimer's disease as early moderators

Contact Info

Product

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Calcium (Ca²⁺) hemostasis, mitochondria, autophagy, and mitophagy contribute to Alzheimer's disease as early moderators