Oxidative stress plays a crucial role in the occurrence and development of osteoarthritis (OA) through the activation of endoplasmic reticulum (ER) stress. Curcumin is a polyphenolic compound with significant antioxidant and anti-inflammatory activity among various diseases. To elucidate the role of curcumin in oxidative stress-induced chondrocyte apoptosis, this study investigated the effect of curcumin on ER stress-related apoptosis and its potential mechanism in oxidative stress-induced rat chondrocytes. The results of flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining showed that curcumin can significantly attenuate ER stress-associated apoptosis. Curcumin inhibited the expression of cleaved caspase3, cleaved poly (ADP-ribose) polymerase (PARP), C/EBP homologous protein (CHOP), and glucose-regulated protein78 (GRP78) and upregulated the chondroprotective protein Bcl2 in TBHP-treated chondrocytes. In addition, curcumin promoted the expression of silent information regulator factor 2-related enzyme 1 (SIRT1) and suppressed the expression of activating transcription factor 4 (ATF4), the ratio of p-PERK/PERK, p-eIF2α/eIF2α. Our anterior cruciate ligament transection (ACLT) rat OA model research demonstrated that curcumin (50 mg/kg and 150 mg/kg) ameliorated the degeneration of articular cartilage and inhibited chondrocyte apoptosis in ACLT rats in a dose-dependent manner. By applying immunohistochemical analysis, we found that curcumin enhanced the expression of SIRT1 and inhibited the expression of CHOP and cleaved caspase3 in ACLT rats. Taken together, our present findings firstly indicate that curcumin could inhibit the PERK-eIF2α-CHOP axis of the ER stress response through the activation of SIRT1 in tert-Butyl hydroperoxide- (TBHP-) treated rat chondrocytes and ameliorated osteoarthritis development in vivo.

Objective: Emerging evidence has indicated that excessive reactive oxygen species (ROS) have detrimental effects on osteoarthritis (OA). This study aimed to elucidate the effects of melatonin (MT), an antioxidant indolamine secreted from the pineal gland, on chondrocyte senescence and cartilage degeneration, thereby clarifying the underlying mechanisms of ROS-induced OA pathogenesis. Design: Hydrogen peroxide (H₂O₂) was used to induce oxidative stress in rat chondrocytes. ROS levels were evaluated using cytometry and immunofluorescence. Cell viability was detected using the Cell Counting Kit-8 (CCK-8) assay. Western blotting and qPCR (Quantiative Real-Time Polymerase Chain Reaction) were used to examine apoptosis and autophagy. For in vivo experiments, male Sprague-Dawley rats were randomly divided into a sham-operated group, DMM (destabilization of the medial meniscus) surgery group, and surgery groups that received melatonin. Knee joints were collected and stained for histological analysis. Results: The data demonstrated that melatonin treatment significantly suppressed H₂O₂-induced matrix degradation and apoptosis, and maintained mitochondrial redox homeostasis. In addition, an enhancement of autophagic flux was observed through western blotting. These findings corresponded with activation of the AMPK/Foxo3 signaling pathways upon melatonin treatment. Histological staining and transmission electron microscopy (TEM) micrographs also demonstrated that melatonin alleviated cartilage ossification and chondrocyte hypertrophy in vivo. Conclusions: Our results indicated that melatonin protected chondrocytes via mitochondrial redox homeostasis and autophagy. The effects of melatonin on senescence may apply to other age-related diseases. Thus, melatonin may have multiple potential therapeutic applications.

Strokes are a major cause of neurological disability. Stem cell replacement therapy is a potential novel strategy of treating patients that have experienced strokes. The present study examined the protective role of neural stem cell (NSC) administration in oxygen‑glucose deprivation (OGD) injury and ischemic stroke animal models. Primary cultured embryonic NSCs and brain microvascular endothelial cells were indirectly co‑cultured for in vitro testing. A rat model of embolic middle cerebral artery occlusion (MCAO) was used to assess the morphological and functional changes that occur following treatment with NSCs. The role of the phosphoinositide 3‑kinase/protein kinase b/glycogen synthase kinase 3β (PI3K/Akt/GSK‑3β) signaling pathway in the neuroprotective effects of NSC treatment was also determined. It was demonstrated in vivo and in vitro that NSC administration may attenuate the brain injury caused by stroke. Furthermore, the results suggest that activation of PI3k/Akt/GSK‑3β signaling pathway serves a role in attenuating OGD injury. Inflammation, synaptic remodeling and autophagy may be improved following NSC treatment and behavioral testing suggests that treatment with NSCs improves functional recovery in rats following MCAO.

The previous anterior approach to the elbow provides a limited exposure of the coronoid process. The aim of this study was to identify the optimal exposure interval for coronoid fractures from the anterior aspect of elbow. We exposed the coronoid process on twelve fresh-frozen cadaveric elbows from the anteromedial aspect of the elbow. The dissection intervals used were the novel brachial artery-median nerve interval (B-M interval) and the previously reported biceps tendon-brachial artery interval (B-B interval). Access to key anatomic landmarks around the coronoid process was assessed and the exposed surface area of coronoid process was calculated in each specimen. The average exposed surface area of coronoid process was 2.26 times greater with the B-M interval (4.58 cm²) compared with the B-B interval (2.03 cm²) (p < 0.05). All key anatomic landmarks around the coronoid process were directly visualised via the B-M interval in each specimen. In conclusion, the anteromedial approach through the B-M interval provides a more extensive exposure of the coronoid process than the traditional B-B interval. This new approach can be useful for the fixation of coronoid fractures.