Morin has protective potential against ER stress induced apoptosis in renal proximal tubular HK-2 cells

Area of Science:

• Nephrology
• Cellular Biology
• Pharmacology

Background:

• Endoplasmic reticulum (ER) stress is an early indicator of acute kidney injury and accelerates chronic kidney disease.
• Compounds that inhibit ER stress may regulate ER stress-induced apoptosis.
• Investigating natural compounds for kidney disease treatment is crucial.

Purpose of the Study:

• To investigate the protective effects of the flavonoid morin against ER stress-induced apoptosis in human renal proximal tubular HK-2 cells.
• To determine if morin can act as an ER stress inhibitor.

Main Methods:

• HK-2 cells were treated with tunicamycin (TM) to induce ER stress.
• The effects of morin pretreatment on ER stress markers (GRP78, IRE1 pathway components like XBP1-sp, phosphor-IRE-1α, phosphor-JNK) were analyzed.
• Intracellular reactive oxygen species (ROS) production and apoptosis were measured.

Main Results:

• Morin downregulated the expression of GRP78, a central ER stress regulator, induced by TM.
• Morin selectively inhibited the IRE1 pathway, suppressing TM-induced increases in XBP1-sp, phosphor-IRE-1α, and phosphor-JNK.
• Morin decreased TM-induced intracellular ROS production and apoptosis in HK-2 cells.

Conclusions:

• Morin demonstrates protective effects against ER stress-induced apoptosis in kidney cells.
• Morin functions as an ER stress inhibitor by modulating the IRE1 pathway.
• Morin is a potential therapeutic candidate for ER-stress-associated kidney diseases.