SAC and Berberine Mediated Repression of Reactive Species and Hepatoprotection After DEN + CCl4 Exposure

Sengupta, Dipanwita; Chatterjee, Sabyasachi; Chatterjee, Tania; Chowdhury, Kaustav Dutta; Bhowmick, Priya; Chakraborti, Udipta; Sarkar, Avik; Paul, Soumosish; Sur, Pradip Kumar; Sadhukhan, Gobinda Chandra

doi:10.1007/s12595-015-0156-5

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“…1 Numerous studies have demonstrated that some pharmaceutical agents can induce liver cancer cell apoptosis by triggering reactive oxygen species (ROS)-mediated endoplasmic reticulum (ER) stress. [2][3][4] However, liver cancer cell heterogeneity and drug resistance pose major obstacles to the treatment of liver cancer. Recent evidence has indicated that nanoparticles conjugated with pharmaceutical agents or genetic vectors can enhance drug sensitivity in cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Titanium dioxide nanoparticles induce endoplasmic reticulum stress-mediated apoptotic cell death in liver cancer cells

et al. 2020

J Int Med Res

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Objective Titanium oxide (TiO2) acts as a photosensitizer in photodynamic therapy by mediating reactive oxygen species (ROS)-induced endoplasmic reticulum (ER) stress. This study aimed to investigate the effect of TiO2 on ER stress in liver cancer cells. Methods Normal human liver and human hepatocarcinoma cell lines were incubated with various concentrations of TiO2 nanotubes for 48 hours. Cell growth, apoptosis, cell cycle, and cellular ROS were detected. Expression levels of ER stress sensors (PERK and ATF6) and Bax were evaluated by western blot. The effect of TiO2 on liver cancer growth was also investigated in mice in vivo. Results TiO2 inhibited cell growth, increased apoptosis and cellular ROS levels, and arrested the cell cycle in G1 stage in liver cancer cells. TiO2 also increased PERK, ATF6, and Bax expression levels in liver cancer cells in dose-dependent manners. TiO2 had no significant effect on cell growth, apoptosis, ROS level, cell cycle distribution, or PERK, ATF6, or Bax expression in normal liver cells. TiO2 administration reduced tumor volume and increased PERK, Bax, and ATF6 expression levels in tumor tissues in vivo. Conclusions TiO2 nanoparticles increased ROS-induced ER stress and activated the PERK/ATF6/Bax axis in liver cancer cells in vitro and in vivo.

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Section: Introductionmentioning

confidence: 99%

Titanium dioxide nanoparticles induce endoplasmic reticulum stress-mediated apoptotic cell death in liver cancer cells

et al. 2020

J Int Med Res

View full text Add to dashboard Cite

show abstract

SAC and Berberine Mediated Repression of Reactive Species and Hepatoprotection After DEN + CCl4 Exposure

Cited by 1 publication

References 55 publications

Titanium dioxide nanoparticles induce endoplasmic reticulum stress-mediated apoptotic cell death in liver cancer cells

Titanium dioxide nanoparticles induce endoplasmic reticulum stress-mediated apoptotic cell death in liver cancer cells

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