10 September 2020: Review Articles
The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human Diseases
Shuangshuang Zhang 1ABCDE* , Mengke Cao 2BCDE* , Fang Fang 3AEFG*DOI: 10.12659/MSM.924558
Med Sci Monit 2020; 26:e924558
Table 2 The role of EGCG in ERS-induced apoptosis and human diseases.
| Disease model | Dose | EGCG Effect | References |
|---|---|---|---|
| Cancer (colorectal cancer cells) | 125, 250, 500, 1000 μM | EGCG upregulated BiP, PERK, phosphorylation eIF2α, ATF4, and IRE1α and increased caspase 3/7 activity | 90 |
| Cancer (mouse hepatoma cells) | 100 μM | EGCG inhibited glucosidase II, increased eIF2α phosphorylation, cleavage of procaspase-12, induction of CHOP/GADD153, and depletion of ER calcium | 92 |
| Cancer (MMe cells) | 5, 10, 50, 100 μM | EGCG improved GRP78, induced EDEM, CHOP, XBP1, ATF4 expressions, and increased the activity of caspase 3 and 8 | 94 |
| Cancer (human glioblastoma T98G and U87MG cells) | 50 μM | EGCG promoted ROS production, induced p38 MAPK phosphorylation, caspase-8 activation, proteolytic cleavage of Bid, and activated JNK pathway | 96 |
| Cancer (human urothelial carcinoma cells) | 10, 20, 33.3, 40 μM | EGCG improved apoptosis by activating CHOP, caspase 4, GRP78, and IRE-1α | 97 |
| Cancer (hepatoma cells) | 20 μM | EGCG overcame chrysin-induced GRP78 expression and potentiated the activation of caspase-7 by chrysin. | 98 |
| Cancer (glioblastoma cells) | 20 μM | EGCG promoted the current treatment effect of temozolomide by reducing GRP78 and upregulating CHOP | 99 |
| Cancer (breast cancer cells) | 10 μM EGCG | EGCG induced PARP cleavage, caspase 7 activation and JNK phosphorylation in breast cancer with vinblastine and Taxol treatment | 100 |
| Cancer (multiple myeloma cells and glioblastoma cells) | 10, 20 μM | EGCG directly reacted with BZM to block the effect of BZM and EGCG prevented proteasome inhibition and ER stress induction | 101 |
| Neurological Diseases (SH-SY5Y cells) | 5, 10, 20 μM | EGCG reduced ERS-induced apoptosis by downregulating cleaved caspase 3 and caspase 12, CHOP, GRP78 | 103 |
| Neurological Diseases (neuronal cells) | 25 μM | EGCG inhibited ERS with decreasing caspase-12, CHOP, and GRP78, and improved the neurological status via inhibiting TRPC6 proteolysis and activating CREB via the MEK/ERK pathway | 105 |
| Neurological Diseases (familial amyloidotic polyneuropathy mice models) | 100 mg kg | EGCG reduced BiP, the phosphorylated eIF2α, protein oxidation marker-3-nitrotyrosine and death receptor Fas | 106 |
| Diabetes (db/db mice) | 10 g kg | EGCG promoted the secretion of insulin and glucose tolerance, reduced the number of Langerhans pathological islets and ERS markers of the islet, increased area and number of islets, and increased the pancreatic endocrine area | 108 |
| Diabetes (Wistar rats) | 200 mg kg | A-type EGCG dimer prevented insulin resistance and hyperglycemia by inhibiting ERS-induced apoptosis, decreasing the levels of G6Pase and PEPCK, and the activities of ATF4, p-JNK, p-IRE1 and p-PERK | 109 |
| Diabetes (podocytes) | 20 μM | EGCG attenuated apoptosis of glucose-induced podocyte through inhibiting ERS with attenuating the expressions of caspase-12, p-PERK and GRP78 | 110 |
| Diabetes (diabetic mice) | 100 mg kg | EGCG reduced apoptosis of testicular cell by ERS, oxidative damage, and inflammation, and activated the expression of NRF2 | 110 |
| Cardiovascular Diseases (endothelial cells) | 10 μM | EGCG enhanced AMPK phosphorylation, suppressed ROS production, TXNIP induction, NLRP3 inflammasome activation and attenuated mitochondrial cell apoptosis. | 112 |
| Adverse Reactions (C57/BL6 mice) | 100 mg kg | EGCG attenuated the CP-induced renal dysfunction, kidney tubular damage, and decreased the expression of phosphorylated ERK, GRP78, and caspase 12 | 114 |
| Injury (Sprague-Dawley rats) | 4.5 mg kg | EGCG improved pBOO-induced histologic changes, bladder dysfunction, and the overexpression of cyclooxygenase-2, CHOP, and caspase-12 | 117 |
| Injury (primary retinal pigment epithelial cells) | 10 μM | EGCG inhibited ERS-mediated apoptosis via downregulating cleaved caspase-12, cleaved caspase-3, cleaved PARP, IRE1α, ERO1α, PERK, CHOP, GRP78, and phosphorylation at ser9 of GSK3β, and upregulating the expression of phosphorylation ser380 of PTEN and ser473 of AKT | 119 |
| EGCG – epigallocatechin-3-gallate; ROS – reactive oxygen species; VEGF – vascular endothelial growth factor; CFRT – cystic fibrosis transmembrane conductance regulator. | |||