Based on PI3K/Akt Signaling Pathway, the Effects of Gubi Decoction on Chondrocyte Proliferation, Apoptosis, and Expression of Inflammatory Factors in a Rat Model of Osteoarthritis.

Objective: Given the crucial role of the PI3K/Akt signaling pathway in chondrocyte survival and inflammation in osteoarthritis (OA), this study aimed to investigate the effects of Gu Bi Tang on chondrocyte proliferation, apoptosis, and inflammatory factor expression in a rat model of OA, with a focus on the PI3K/Akt signaling pathway.

Methods: Forty-five specific pathogen-free (SPF) C57 mice were randomly divided into three groups: the model group (Group A), the Gu Bi Tang group (Group B), and the Amfenac group (Group C), with 15 rats in each group. All 45 rats underwent anterior cruciate ligament transection (ACLT) surgery to establish an OA model.

Sema3A ameliorates the pathological progression of osteoarthritis by modulating mitochondrial damage in chondrocytes.

Osteoarthritis (OA) is a major disease that causes disability in middle-aged and elderly people. A comprehensive understanding of its pathogenesis is of great significance in finding new clinical diagnosis and treatment schemes. The role of Semaphorin 3A (Sema3A) in OS has attracted attention recently, and the purpose of this study is to analyze the mechanisms underlying its impact on OS.

Apolipoprotein E2 inhibits mitochondrial apoptosis in pancreatic cancer cells through ERK1/2/CREB/BCL-2 signaling.

Background: Apolipoprotein E2 (ApoE2) is a pleiotropic protein that influences several aspects of cancer metabolism and development. Evading apoptosis is a vital factor for facilitating cancer cell growth. However, the role and mechanism of ApoE2 in regulating cell apoptosis of pancreatic cancer remain unclear.

Semaphorin3A regulates mitochondrial apoptosis in RAW264.7 cells in vitro.

Osteoclasts apoptosis plays vital roles in abnormal bone remodeling-associated diseases. It's reported that Semaphorin3A (Sema3A) may affect osteoarthritis progression through osteoclasts function, while the specific mechanism remains unclear. To determine the effect of Sema3A on osteoclasts, we detected the apoptosis of RAW264.

Astrocytes directly clear myelin debris through endocytosis pathways and followed by excessive gliosis after spinal cord injury.

Persisted myelin debris inhibit axon regeneration and contribute to further tissue damage after spinal cord injury (SCI). The traditional view is that myelin debris is mainly cleared by microglia and macrophages, while astrocytes cannot directly engulf myelin debris because they are absent from lesion core. Here, we definitely showed that astrocytes could directly uptake myelin debris both in vitro and in vivo to effectively complement the clearance function.

Bone-Derived Extracellular Vesicles: Novel Players of Interorgan Crosstalk.

An increasing number of studies have shown that bone plays an active role in regulating glucose metabolism, affects renal, and cardiovascular diseases and even influences the development of offspring. These novel findings have indicated that bone plays a much more important role in the human body than only providing physical support. However, further investigations of the mechanisms underlying the effects of bone are needed.

Tenascin-C Modulates Cell Cycle Progression to Enhance Tumour Cell Proliferation through AKT/FOXO1 Signalling in Pancreatic Cancer.

Pancreatic ductal adenocarcinoma (PDAC) is a disease with an extremely poor prognosis that is characterized by a rich extracellular matrix (ECM). Tenascin-C (TNC) is a component of the ECM and plays a role in tumour progression. In this study, we reported that TNC is overexpressed in PDAC tissues and is correlated with tumour stage and cyclin D1 expression.

Tenascin-C induces migration and invasion through JNK/c-Jun signalling in pancreatic cancer.

Tenascin-C (TNC), a large extracellular matrix glycoprotein, has been reported to be associated with metastasis and poor prognosis in pancreatic cancer. However, the effects and mechanisms of TNC in pancreatic cancer metastasis largely remain unclear. We performed Transwell assays to investigate the effects of TNC on Capan-2, AsPC-1 and PANC-1 cells.

Fractalkine/CX3CR1 induces apoptosis resistance and proliferation through the activation of the AKT/NF-κB cascade in pancreatic cancer cells.

Fractalkine (FKN, CX3CL1) is highly expressed in a majority of malignant solid tumours. Fractalkine is the only known ligand for CX3CR1. In this study, we performed an analysis to determine the effects of fractalkine/CX3CR1 on modulating apoptosis and explored the related mechanisms.