Tetrahydrohyperforin prevents articular cartilage degeneration and affects autophagy in rats with osteoarthritis

Zhang, Jinling; Wang, Sisheng; Rong, Genxiang; Cheng, Fangyue; Gui, Binjie; Shen, Cailiang

doi:10.3892/etm.2018.6098

Cited by 7 publications

(9 citation statements)

References 59 publications

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“…Zhang et al . discovered that tetrahydrohyperforin could improve the pathological severity of a joint injury in a rat model that was chemically induced by intra-articular injection of collagenase solution [ 148 ]. The role of autophagy regulation in chondrocytes by tetrahydrohyperforin should be further investigated in PTOA models.…”

Section: Reviewmentioning

confidence: 99%

Autophagy in the pathogenesis and therapeutic potential of post-traumatic osteoarthritis

Gong

et al. 2023

Burns &Amp; Trauma

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Autophagy, as a fundamental mechanism for cellular homeostasis, is generally involved in the occurrence and progression of various diseases. Osteoarthritis (OA) is the most common musculoskeletal disease that often leads to pain, disability and economic loss in patients. Post-traumatic OA (PTOA) is a subtype of OA, accounting for >12% of the overall burden of OA. PTOA is often caused by joint injuries including anterior cruciate ligament rupture, meniscus tear and intra-articular fracture. Although a variety of methods have been developed to treat acute joint injury, the current measures have limited success in effectively reducing the incidence and delaying the progression of PTOA. Therefore, the pathogenesis and intervention strategy of PTOA need further study. In the past decade, the roles and mechanisms of autophagy in PTOA have aroused great interest in the field. It was revealed that autophagy could maintain the homeostasis of chondrocytes, reduce joint inflammatory level, prevent chondrocyte death and matrix degradation, which accordingly improved joint symptoms and delayed the progression of PTOA. Moreover, many strategies that target PTOA have been revealed to promote autophagy. In this review, we summarize the roles and mechanisms of autophagy in PTOA and the current strategies for PTOA treatment that depend on autophagy regulation, which may be beneficial for PTOA patients in the future.

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Section: Reviewmentioning

confidence: 99%

Autophagy in the pathogenesis and therapeutic potential of post-traumatic osteoarthritis

Gong

et al. 2023

Burns &Amp; Trauma

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“…Autophagy in the knee cartilage tissue was assessed by TEM as previously described. 20 Briefly, knee cartilage tissue was fixed in 2.5% glutaraldehyde and post-fixed in 1% osmium tetroxide. Then the tissue was dehydrated in ethyl alcohol and embedded in Epon.…”

Section: Autophagy Observed Via Transmission Electron Microscopymentioning

confidence: 99%

“…Total proteins were extracted from exosomes, wholecell lysates, or homogenized knee cartilage tissue using the radioimmunoprecipitation assay lysis buffer (Beyotime, Haimen, China) and then subjected to western blot as previously described. 20 The primary antibodies were as follows: Alix (1:1,000; Abcam), CD63 (1:1,000; Abcam), ATF4 (1:1,000; Abcam), microtubule-associated protein 1 light chain 3 (LC3)-I and LC3-II (both from anti-LC3B antibodies, 1:1,000; Abcam), ATG5 (1:1,000; Abcam), MMP13 (1:1,000; Abcam), COL-II (1:1000; Invitrogen), and β-actin (1:1,000; Abcam). The signals were visualized using an ECL chemiluminescent system (Pierce).…”

Section: Western Blotmentioning

confidence: 99%

ATF4‐modified serum exosomes derived from osteoarthritic mice inhibit osteoarthritis by inducing autophagy

Wang

Liang

et al. 2020

IUBMB Life

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Activating transcription factor 4 (ATF4) is critical for chondrocyte proliferation and bone formation. Exosomes are considered as promising gene-delivery vehicles for the treatment of osteoarthritis (OA). This study utilized the serum-derived exosomes from OA mice as the gene-delivery vehicles for ATF4 gene therapy and explored their therapeutic effects on OA. Meniscus injury-induced OA model was established by the excision of anterior part of medial meniscus in the right knee of C57BL/6J mice. Exosomes were isolated from serum samples of sham and OA mice, and were referred to as sham-Exo and OA-Exo, respectively. ATF4-overexpressing OA-Exo (ATF4-OA-Exo) was developed by introducing ATF4 mRNA into OA-Exo via electroporation. Four weeks after surgery, OA mice received intra-articular injections of sham-Exo, OA-Exo, and ATF4-OA-Exo, respectively. The results showed that intra-articular injection of ATF4-OA-Exo alleviated articular cartilage degeneration or damage and inflammatory response of OA mice. Autophagy was weakened in knee joint cartilage of OA mice, which was partially restored by intra-articular injection of ATF4-OA-Exo. Further in vitro assays revealed that ATF4-OA-Exo promoted chondrocyte autophagy and inhibited chondrocyte apoptosis in the TNF-α-or tunicamycin-treated chondrocytes. Together, ATF4-modified serum exosomes derived from OA mice protect cartilage and alleviate OA progression by inducing autophagy.

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“…29-31 Moreover, when the level of autophagy was reduced, the occurrence and development of knee OA were also more rapid. 32-34 Targeted deletion of Atg-5 in chondrocytes promotes age-related OA. Notably, because chondrocytes exist in nutrient-poor medium, energy intake is essential for their survival.…”

Section: Introductionmentioning

confidence: 99%

Loss of Autophagy Causes Increased Apoptosis of Tibial Plateau Chondrocytes in Guinea Pigs with Spontaneous Osteoarthritis

Wang

Tian

Xu³

et al. 2021

CARTILAGE

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Objective The goal of the present study was to observe the effect of autophagy in tibial plateau chondrocytes on apoptosis in spontaneous knee osteoarthritis (OA) in guinea pigs. Design Fifty 2-month-old female Hartley guinea pigs were divided into a normal group (10 animals, all euthanized after 7 months) and an OA group (40 animals, 10 of which were euthanized after 10 months). Immunohistochemistry, RT-qPCR and Western blotting were used to evaluate autophagy levels, intracellular glycogen accumulation and apoptosis in tibial plateau chondrocytes in vivo and in vitro. The remaining 30 guinea pigs in the OA group were divided into 3 groups: a rapamycin group, a normal saline group, and a 3-methyladenine (3-MA) group. Intracellular glycogen accumulation and chondrocyte apoptosis were assessed by altering the level of autophagy in chondrocytes in vivo. Results When spontaneous OA occurred in guinea pigs, autophagy levels in tibial plateau chondrocytes decreased, while intracellular glycogen accumulation and the rate of chondrocyte apoptosis increased. After enhancing the level of autophagy in tibial plateau chondrocytes in guinea pigs with OA, intracellular glycogen accumulation and the rate of chondrocyte apoptosis decreased, while inhibiting autophagy had the opposite effects. Conclusion The results indicate that the function of autophagy in chondrocytes may at least partly involve the catabolism of glycogen. In guinea pigs with OA, the level of autophagy in tibial plateau chondrocytes decreased, and chondrocytes were unable to degrade intracellular glycogen into glucose, leading to less energy for chondrocytes and increased apoptosis.

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Tetrahydrohyperforin prevents articular cartilage degeneration and affects autophagy in rats with osteoarthritis

Cited by 7 publications

References 59 publications

Autophagy in the pathogenesis and therapeutic potential of post-traumatic osteoarthritis

Autophagy in the pathogenesis and therapeutic potential of post-traumatic osteoarthritis

ATF4‐modified serum exosomes derived from osteoarthritic mice inhibit osteoarthritis by inducing autophagy

Loss of Autophagy Causes Increased Apoptosis of Tibial Plateau Chondrocytes in Guinea Pigs with Spontaneous Osteoarthritis

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