Abstract
Salvianolic acid B is an antioxidative ingredient derived from Radix Salviae miltiorrhizae that has been widely used to treat liver diseases. However, the therapeutic mechanism underlying Salvianolic acid B has remained largely unknown. Our studies verified that Salvianolic acid B efficiently blocked mitochondrial deformation and dysfunction induced by H2O2 in the human hepatocyte cell line HL7702. Mortalin, a mitochondrial molecular chaperone, maintains mitochondrial morphology stabilization and function integrity. Previous results showed that mortalin overexpression has been observed in hematoma carcinoma cells and that mortalin maintains mitochondrial homeostasis and antagonizes oxidative stress damage. We found that Salvianolic acid B significantly up-regulated mortalin protein expression levels. In addition, Salvianolic acid B lost the function of preventing mitochondrial deformation and dysfunction induced by oxidative stress under mortalin knockdown conditions. We further found that mortalin overexpression increases the mRNA expression of mitofusin-related factor Mfn1 and mitofission-related factor hFis1. In conclusion, Salvianolic acid B maintains the mitochondrial structure stabilization and functional integrity by up-regulating mortalin, which may be associated with increased mitofusin factor Mfn1 and reduced mitofission factor hFis1.
Highlights
IntroductionMortalin (mtHsp70/Hsp75/Grp75/PBP74) is a heat un-inducible protein that is a heat shock protein 7 (Hsp70) family member
Mortalin is a heat un-inducible protein that is a heat shock protein 7 (Hsp70) family member
Pretreatment with SalB remarkably scavenges free radicals, maintains mitochondrial membrane permeability, guarantees energy basal metabolism, and inhibits the activation of apoptotic-related factors, indicating that the antioxidant properties of SalB notably rescue the mitochondrial dysfunction caused by H2O2-induced oxidative stress, which is consistent with other reports[3,35,36]
Summary
Mortalin (mtHsp70/Hsp75/Grp75/PBP74) is a heat un-inducible protein that is a heat shock protein 7 (Hsp70) family member. Mortalin is located predominantly in mitochondria, where it functions to maintain mitochondrial homeostasis and quality control[16,17]. Previous studies show that mortalin overexpression inhibits cell apoptosis by attenuating/reducing accumulation of ROS during various forms of stresses[20,21]. Mortalin knockdown is effective in mitochondrial dynamics. Mortalin induces mitochondrial fission by regulating the balance of mitochondrial dynamics[22]. This study primarily focuses on investigating the effects of SalB on mitochondrial homeostasis and the balance of mitochondrial dynamics and testing whether mortalin can protect against mitochondrial dysfunction by regulating the balance of mitochondrial dynamics under H2O2-induced oxidative stress. We studied the possible mechanisms of SalB mitochondrial protection by assessing the correlation with mortalin
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