Proteomic Analysis of Staphylococcus aureus Treated with ShangKeHuangShui.

Staphylococcus aureus (SAU) stands as the prevailing pathogen in post-traumatic infections, with the emergence of antibiotic resistance presenting formidable treatment hurdles. The pressing need is to explore novel antibiotics to address this challenge. ShangKeHuangShui (SKHS), a patented traditional Chinese herbal formula, has gained widespread use in averting post-traumatic infections, but its biological effects remain incomplete understanding.

Effects of aligned PLGA/SrCSH composite scaffolds on in vitro growth and osteogenic differentiation of human mesenchymal stem cells.

Strontium (Sr) has important functions in bone remodeling. Incorporating strontium-doped α-calcium sulfate hemihydrate (SrCSH) into poly(lactic-co-glycolic acid) (PLGA) fibrous scaffolds were expected to increase its bio-activity and provide a potential material for bone tissue engineering. In the present study, Sr-containing aligned PLGA/SrCSH fibrous scaffolds similar to the architecture of natural bone were prepared via wet spinning.

SSR1 and CKAP4 as potential biomarkers for intervertebral disc degeneration based on integrated bioinformatics analysis.

Background: Intervertebral disc degeneration (IDD) is a significant cause of low back pain and poses a significant public health concern. Genetic factors play a crucial role in IDD, highlighting the need for a better understanding of the underlying mechanisms.

Aim: The aim of this study was to identify potential IDD-related biomarkers using a comprehensive bioinformatics approach and validate them in vitro.

Coptisine Inhibits Influenza Virus Replication by Upregulating p21.

The activation of innate antiviral immunity is a promising approach for combatting viral infections. In this study, we screened Chinese herbs that activated human immunity and identified coptisine as a potent inhibitor of the influenza virus with an EC of 10.7 μM in MDCK cells.

Identification of Andrographolide as a novel FABP4 inhibitor for osteoarthritis treatment.

Background And Purpose: Fatty acid binding protein 4 (FABP4) has been identified as a contributor to cartilage degradation in osteoarthritis (OA) patients, and inhibiting FABP4 using small molecules has emerged as a promising approach for developing OA drugs. Our previous research showed that Andrographis paniculata, a medicinal plant, strongly inhibits FABP4 activity. This led us to hypothesize that Andrographis paniculata ingredients might have protective effects on OA cartilage through FABP4 inhibition.

Shang-Ke-Huang-Shui and coptisine alleviate osteoarthritis in the knee of monosodium iodoacetate-induced rats through inhibiting CXCR4 signaling.

Ethnopharmacological Relevance: Shang-Ke-Huang-Shui (SKHS) is a classic traditional Chinese medicine formula originally from the southern China city of Foshan. It has been widely used in the treatment of osteoarthritis (OA) but underlying molecular mechanisms remain unclear.

Aim Of Study: Recently, activation of C-X-C chemokine receptor type 4 (CXCR4) signaling has been reported to induce cartilage degradation in OA patients; therefore, inhibition of CXCR4 signaling has becoming a promising approach for OA treatment.

Liquid crystalline matrix-induced viscoelastic mechanical stimulation modulates activation and phenotypes of macrophage.

Accumulating evidence indicates that the mechanical microenvironment exerts profound influences on inflammation and immune modulation, which are likely to be key factors in successful tissue regeneration. The elastic modulus (Em) of the matrix may be a useful adjustable property to control macrophage activation and the overall inflammatory response. This study constituted a series of Em-tunable liquid crystalline cell model (HpCEs) resembling the viscoelastic characteristic of ECM and explored how mechanical microenvironment induced by liquid crystalline soft matter matrix affected macrophage activation and phenotypes.

Predicting and Anti-SARS-CoV-2 Activities of Antivirals by Intracellular Bioavailability and Biochemical Activity.

Cellular drug response (concentration required for obtaining 50% of a maximum cellular effect, EC) can be predicted by the intracellular bioavailability ( ) and biochemical activity (half-maximal inhibitory concentration, IC) of drugs. In an ideal model, the cellular negative log of EC (pEC) equals the sum of log and the negative log of IC (pIC). Here, we measured 's of remdesivir, favipiravir, and hydroxychloroquine in various cells and calculated their anti-SARS-CoV-2 EC's.

Astragaloside IV as a novel CXCR4 antagonist alleviates osteoarthritis in the knee of monosodium iodoacetate-induced rats.

Background And Purpose: C-X-C chemokine receptor type 4 (CXCR4) inhibition protects cartilage in osteoarthritis (OA) animal models. Therefore, CXCR4 has becoming a novel target for OA drug development. Since dietary and herbal supplements have been widely used for joint health, we hypothesized that some supplements exhibit protective effects on OA cartilage through inhibiting CXCR4 signaling.

Glycyrrhizin Inhibits SARS-CoV-2 Entry into Cells by Targeting ACE2.

Coronavirus Disease 2019 (COVID-19) is a highly infectious and pathogenic disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Early in this epidemic, the herbal formulas used in traditional Chinese medicine (TCM) were widely used for the treatment of COVID-19 in China. According to Venn diagram analysis, we found that is a frequent herb in TCM formulas against COVID-19.

[Acupoint puncture combined with Ilizarov technique for the treatment of elderly paitents with knee osteoarthritis].

Objective: To explore the clinical effect of acupoint puncture combined with Ilizarov technique in the treatment of knee osteoarthritis in the elderly.

Methods: From March 2015 to February 2016, 76 patients with primary knee osteoarthritis were treated with tibial osteotomy acupoint puncture grouop and Ilizarov technique anatomical puncture group, including 24 males and 52 females, aged 56 to 75 years old with an average of 61.4 years old, and a course of 3 to 17 years with an average of 5.

Nutlin-3 treatment spares cisplatin-induced inhibition of bone healing while maintaining osteosarcoma toxicity.

The majority of Osteosarcoma (OS) patients are treated with a combination of chemotherapy, resection, and limb salvage protocols. These protocols include distraction osteogenesis (DO), which is characterized by direct new bone formation. Cisplatin (CDP) is extensively used for OS chemotherapy and recent studies, using a mouse DO model, have demonstrated that CDP has profound negative effects on bone repair.

Cisplatin inhibits bone healing during distraction osteogenesis.

Osteosarcoma (OS) is the most common malignant bone tumor affecting children and adolescents. Many patients are treated with a combination of chemotherapy, resection, and limb salvage protocols. Surgical reconstructions after tumor resection include structural allografts, non-cemented endoprostheses, and distraction osteogenesis (DO), which require direct bone formation.

Osteo-promoting effects of insulin-like growth factor I (IGF-I) in a mouse model of type 1 diabetes.

Objective: Using a streptozotocin (STZ)-induced mouse model of type 1 diabetes (T1D), we have previously demonstrated that long-term diabetes inhibits regenerative bone formation during tibial distraction osteogenesis (DO) and perturbs skeletal integrity by decreasing cortical thickness, bone mineral density and bone's resistance to fracture. Because long-standing T1D is also associated with a deficiency of insulin-like growth factor I (IGF-I), we examined the effects of systemic IGF-I treatment on skeletal microarchitecture and strength, as well as on bone formation in diabetic mice.

Research Design And Methods: Streptozotocin-induced diabetic or control mice were treated with recombinant human IGF-I (rhIGF-I, 1.

Rosiglitazone disrupts endosteal bone formation during distraction osteogenesis by local adipocytic infiltration.

Rosiglitazone (Rosi) is a drug in the thiazolidinedione class for treatment of type 2 diabetes mellitus (T2DM), which binds and activates PPARγ nuclear receptor in fat cells, sensitizing them to insulin. Despite proven antidiabetic efficacy, Rosi therapy may be associated with trabecular bone loss and an increased risk of fractures. To examine the potential side effects of Rosi treatment on bone formation, we delivered Rosi to mice using a combined model of distraction osteogenesis (DO) and type 2 diabetes mellitus (T2DM).

Rosiglitazone inhibits bone regeneration and causes significant accumulation of fat at sites of new bone formation.

Thiazolidinediones (TZDs), peroxisome proliferator-activated receptor gamma activators, and insulin sensitizers represent drugs used to treat hyperglycemia in diabetic patients. Type 2 diabetes mellitus (T2DM) is associated with a twofold increase in fracture risk, and TZDs use increases this risk by an additional twofold. In this study, we analyzed the effect of systemic administration of the TZD rosiglitazone on new bone formation in two in vivo models of bone repair, a model of drilled bone defect regeneration (BDR) and distraction osteogenesis (DO) and a model of extended bone formation.

Distraction osteogenesis in TNF receptor 1 deficient mice is protected from chronic ethanol exposure.

Distraction osteogenesis (DO) is an orthopedic protocol, which induces direct new bone formation as a result of the stimulating effects of mechanical distraction. Chronic ethanol exposure has been demonstrated to inhibit bone formation in rodent models of DO. Further, it has been demonstrated that (1) tumor necrosis factor-α (TNF) blockers are protective against ethanol exposure and (2) recombinant mouse TNF (rmTNF) inhibits direct bone formation in ethanol naïve mice through TNF receptor 1 (TNFR1).

Direct bone formation during distraction osteogenesis does not require TNFalpha receptors and elevated serum TNFalpha fails to inhibit bone formation in TNFR1 deficient mice.

Distraction osteogenesis (DO) is a process which induces direct new bone formation as a result of mechanical distraction. Tumor necrosis factor-alpha (TNF) is a cytokine that can modulate osteoblastogenesis. The direct effects of TNF on direct bone formation in rodents are hypothetically mediated through TNF receptor 1 and/or 2 (TNFR1/2) signaling.

Restoration of regenerative osteoblastogenesis in aged mice: modulation of TNF.

Skeletal changes accompanying aging are associated with both increased risk of fractures and impaired fracture healing, which, in turn, is due to compromised bone regeneration potential. These changes are associated with increased serum levels of selected proinflammatory cytokines, e.g.

Runt-related transcription factor 2 (RUNX2) and RUNX2-related osteogenic genes are down-regulated throughout osteogenesis in type 1 diabetes mellitus.

Type 1 diabetes mellitus is associated with a number of disorders of skeletal health, conditions that rely, in part, on dynamic bone formation. A mouse model of distraction osteogenesis was used to study the consequences of streptozotocin-induced diabetes and insulin treatment on bone formation and osteoblastogenesis. In diabetic mice compared with control mice, new bone formation was decreased, and adipogenesis was increased in and around, respectively, the distraction gaps.

A novel rat model for the study of deficits in bone formation in type-2 diabetes.

Background: There is evidence to suggest that impairment in bone formation and/or turnover is associated with the metabolic abnormalities characteristic of type-2 diabetes mellitus. However, bone regeneration/repair in type-2 diabetes has not been modeled. Using Zucker Diabetic Fatty (ZDF) rats (a model of type-2 diabetes) for tibial distraction osteogenesis (DO), we hypothesized that bone formation within the distraction gap would be impaired.

Chronic ethanol exposure inhibits distraction osteogenesis in a mouse model: role of the TNF signaling axis.

Tumor necrosis factor-alpha (TNF-alpha) is an inflammatory cytokine that modulates osteoblastogenesis. In addition, the demonstrated inhibitory effects of chronic ethanol exposure on direct bone formation in rats are hypothetically mediated by TNF-alpha signaling. The effects in mice are unreported.