Effects of endoplasmic reticulum stress in cartilage tissue of knee osteoarthritis on the secretion of inflammation molecules and bone metabolism molecules

Objective: To study the effects of endoplasmic reticulum stress in cartilage tissue of knee osteoarthritis (OA) on the secretion of inflammation molecules and bone metabolism molecules. Methods: The patients who received joint replacement in our hospital due to knee osteoarthritis between June 2013 and February 2017 were enrolled as the OA group, and the patients who received knee replacement in our hospital due to trauma during the same period were enrolled as the control group. During the operation, articular cartilage tissue was collected to measure the expression of endoplasmic reticulum stress genes as well as the secretion of inflammation molecules and bone metabolism molecules. Results: PRKR-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme 1 (IRE1), activating transcription factor 6 (ATF6), CCAAT/enhancer-binding protein homologous protein (CHOP) and cysteinyl aspartate specific proteinase-12 (caspase-12) mRNA expression as well as interleukin-1β (IL-1β), IL-6, CXC chemokine ligand 12 (CXCL12), Chemerin, human cartilage glycoprotein-39 (YKL-40), matrix metalloproteinase 13 (MMP13) and receptor activator for nuclear factor-κB ligand (RANKL) secretion in articular cartilage of OA group were obviously higher than those of control group whereas osteoprotegerin (OPG), osteocalcin (OC), collagen-I (COL-I) and COL-III secretion were obviously lower than those of control group, and PERK, IRE1, ATF6, CHOP and Caspase-12 mRNA expression were positively correlated with IL-1β, IL-6, CXCL12, Chemerin,YKL-40, MMP13 and RANKL, and negatively correlated with OPG, OC, COL-I and COL-III. Conclusion: The over-activation of endoplasmic reticulum stress in knee OA cartilage tissue is related to the inflammatory response activation and bone metabolism disorder.

Regulating effects of mangiferin on oxidative stress response and mitochondrial pathway apoptosis in spinal cord injury model

Objective:To study the regulating effects of mangiferin on oxidative stress response and mitochondrial pathway apoptosis in spinal cord injury model.Methods: SD rats were selected as the experimental animals and divided into the control group that underwent sham operation, the injury group that were made into spinal cord injury models and the mangiferin group that were made into spinal cord injury models and given mangiferin intervention. 30 d after the intervention, spinal cord tissue was collected, radioimmunoprecipitation kit was used to determine the contents of oxidative stress indexes ROS, H2O2, SOD, GSH-Px and CAT, and enzyme-linked immunosorbent assay kit was used to determine the contents of apoptosis indexes SKIP, ASK1, Fas, tBid, APAF-1 and Caspase-3.Results:ROS, H2O2, SKIP, ASK1, Fas, tBid, APAF-1 and caspase-3 contents in spinal cord tissue of injury group were significantly higher than those of control group whereas SOD, GSH-Px and CAT contents were significantly lower than those of control group;ROS, H2O2, SKIP, ASK1, Fas, tBid, APAF-1 and caspase-3 contents in spinal cord tissue of mangiferin group were significantly lower than those of injury group whereas SOD, GSH-Px and CAT contents were significantly higher than those of injury group.Conclusion:Mangiferin has inhibitory effect on oxidative stress response and mitochondrial pathway apoptosis in spinal cord injury model.