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Table 1 Anti-tumoral effects of resveratrol in glioblastoma radiotherapy/chemotherapy

From: Therapeutic potentials of resveratrol in combination with radiotherapy and chemotherapy during glioblastoma treatment: a mechanistic review

Model Cell line(s) Resveratrol dosage; route of administration Exposure conditions of RT Chemotherapeutic drug; dosage; route of administration Co-treatment outcomes Refs.
In vitro U-87MG 20 µM 5 Gy; 180 KV X-rays Induction of a delay in cell cycle progression, enhancement of GJIC [82]
In vitro and in vivo CD133 100 µM 2, 4, 6, 8, and 10 Gy; 1.25 MeV (cobalt-60 γ-rays) Induction of apoptosis, suppression of STAT3 signaling, ↑survival rate [70]
In vitro and in vivo SU-2 75 µmol/L (for in vitro) and 150 mg/kg/day (for in vivo); ip 2, 4 and 6 Gy; 6 MV X-rays ↑radiosensitivity, prevention of self-renewal and stemness, ↑apoptosis, induction of autophagy, inhibition of DNA repair [101]
In vitro U87MG 20 µM 2 Gy; 1.25 MeV (cobalt-60 γ-rays) ↓colony number, ↑DNA damage, ↑radiosensitivity [100]
In vitro DBTRG 50 µM Paclitaxel; 50 µM ↑mitochondrial ROS levels, ↑activation of TRPM2 channel, ↑caspase 3 activity, ↑influx of Ca2+ into the cell through TRPM2 channel [108]
In vitro T98G 100 µM Temozolomide; 100 µM ↑chemosensitivity, ↑apoptotic morphology (such as nuclear and cytoplasmic condensation and chromatin aggregation), ↑cleavage of caspase-3, ↓intracellular level and nuclear translocation of NF-κB, repression of MGMT expression [120]
In vitro and in vivo GIC400 andGIC411 20 and 40 µM (for in vitro) and 12.5 mg/kg/day (for in vivo); ip Temozolomide; 200 and 400 µM (for in vitro) and 68 mg/kg/day (for in vivo); oral ↓cell viability, induction of apoptosis, activation of DSBs/pATM/pATR/p53 pathway, inhibition of self-renewal capacity and promotion of cell differentiation, inactivation of STAT3, inhibition of tumor growth [119]
In vitro and in vivo T98G and U138 2, 4, 8, 10, 16 and 32 µM (for in vitro) and 10 mg/kg/day; ip Temozolomide; 400 µM (for in vitro) and 25 mg/kg//day (for in vivo); ip ↓cell viability and proliferation, ↑apoptosis (↑Cleaved caspase-3 and Bax, ↓XIAP and Bcl‐2), suppression of Wnt signaling pathway, downregulation of MGMT expression [121]
In vitro RG-2, LN-18 and LN-428 25, 50, 75 and 100 µM Temozolomide; 250, 500, 750 and 1000 µM Inhibition of growth cell, down-regulation of MGMT overexpression, ↓expression of STAT3, ↓survivin and Bcl-2 levels, Inhibition of STAT3/Bcl-2/survivin signaling pathway [122]
In vitro and in vivo SHG44 10 µM (for in vitro) and 40 mg/kg/day (for in vivo); oral Temozolomide; 100 µM (for in vitro) and 68 mg/kg/day (for in vivo); oral Induction of cell cycle arrest in the G2/M phase, ↑expression of GFAP, down-regulation of MMP-9 expression, inhibition of cell migration, ↑ROS production, activation of AMPK, inhibition of mTOR signaling, down-regulation of Bcl-2, ↓tumor volume, ↓Ki-67 expression [133]
In vitro and in vivo U87 MG 10 µM (for in vitro) and 12.5 mg/kg/day (for in vivo); ip Temozolomide; 100–400 µM (for in vitro) and 10 mg/kg/day (for in vivo); ip ↓autophagy, ↑apoptosis, ↓cell viability, ↑chemosensitivity,↑cell death, ↓tumor volume, ↓ERK activity and LC3-II protein levels, ↑cleavage of PARP [172]
In vitro U87, U138 and U251 30 µM Temozolomide; 100 µM ↑autophagy, abrogation of temozolomide-induced G2 arrest, ↑gammaH2AX, pATM and pChk2, ↑cyclin B and pRb levels, ↓pWee1 and pCdk1 levels, induction of mitotic catastrophe (aberrant chromosome condensation and mitotic phenotype, micronuclei and nuclearfragmentation, abnormal/triple mitosis, ↑percentages of irregular nuclei and large nuclei), ↓clonogenic growth, ↑senescence [163]
In vitro and in vivo U251MG and C6 7.5, 15 and 30 µM and 10 mg/kg/day; ip Temozolomide; 10 mg/kg/day and thrice a week; ip Inhibition of temozolomide-induced autophagy and promotion of apoptosis (up to 15 µM resveratrol), inhibition of ERK1/2-dependent autophagy [164]
  1. ↑, Increase; ↓, Decease; GJIC, Gap junction intercellular communication; MGMT, O6-methylguanine-DNA methyltransferase; STAT3, signal transducer and activator of transcription 3; GFAP, Glial fibrillary acid protein; MMP-9, matrix metalloproteinase-9; ERK, Extracellular signal-regulated kinase; PARP, poly(ADP-ribose) polymerase; ROS, reactive oxygen species