Background: Kalkitoxin (KT) is an active lipopeptide isolated from the cyanobacterium Lyngbya majuscula found in the bed of the coral reef. Although KT suppresses cell division and inflammation, KT’s mechanism of action in vascular smooth muscle cells (VSMCs) is unidentified. Therefore, our main aim was to investigate the impact of KT on vascular calcification for the treatment of cardiovascular disease. Objectives: Using diverse calcification media, we studied the effect of KT on VSMC calcification and the underlying mechanism of this effect. Methods: VSMC was isolated from the 6 weeks ICR mice. Then VSMCs were treated with different concentrations of KT to check the cell viability. Alizarin red and von Kossa staining were carried out to examine the calcium deposition on VSMC. Thoracic aorta of 6 weeks mice were taken and treated with different concentrations of KT, and H and E staining was performed. Real-time polymerase chain reaction and western blot were performed to examine KT’s effect on VSMC mineralization. Calcium deposition on VSMC was examined with a calcium deposition quantification kit. Results: Calcium deposition, Alizarin red, and von Kossa staining revealed that KT reduced inorganic phosphate-induced calcification phenotypes. KT also reduced Ca++ -induced calcification by inhibiting genes that regulate osteoblast differentiation, such as runtrelated transcription factor 2 (RUNX-2), SMAD family member 4, osterix, collagen 1α, and osteopontin. Also, KT repressed Ca2+ -induced bone morphogenetic protein 2, RUNX-2, collagen 1α, osteoprotegerin, and smooth muscle actin protein expression. Likewise, Alizarin red and von Kossa staining showed that KT markedly decreased the calcification of ex vivo ring formation in the mouse thoracic aorta. Conclusions This experiment demonstrated that KT decreases vascular calcification and may be developed as a new therapeutic treatment for vascular calcification and arteriosclerosis.

Vitiligo is a type of chronic autoimmune skin disorder that is highly unpredictable. Houttuynia cordata Thunb. (HC) is a natural compound with several pharmacological properties; however, the fundamental mechanisms of HC effects on Vitiligo have yet to be fully understood. This study aimed to evaluate the effects of HC on the oxidative injury of melanocytes in vivo and in vitro. This study demonstrated that compounds significantly prevented the hydrogen peroxide (H2O2 )-induced B16F10 cell loss of viability and melanin synthesis; in addition, cell apoptosis-regulating of melanocytes significantly decreased, and the expression level of TRP-1 and MITF increased dose-dependently. In animal experiments, C57BL/6 mice received 5% hydroquinone (HQ) for 5 weeks and were treated with HC for 2 weeks. HQ-stimulated vitiligo in mice also produced melanocyte and melanosome degradation. The melanin content and tyrosinase activity of the mice (skin) that received the HC group significantly increased compared to the untreated and 8-methoxyprosalen (8-MOP) groups. These experiments suggest that the HC has potential protective and therapeutic effects for vitiligo.

Vitiligo is a type of chronic autoimmune skin disorder that is highly unpredictable. Houttuynia cordata Thunb. (HC) is a natural compound with several pharmacological properties; however, the fundamental mechanisms of HC effects on Vitiligo have yet to be fully understood. This study aimed to evaluate the effects of HC on the oxidative injury of melanocytes in vivo and in vitro. This study demonstrated that compounds significantly prevented the hydrogen peroxide (H2O2 )-induced B16F10 cell loss of viability and melanin synthesis; in addition, cell apoptosis-regulating of melanocytes significantly decreased, and the expression level of TRP-1 and MITF increased dose-dependently. In animal experiments, C57BL/6 mice received 5% hydroquinone (HQ) for 5 weeks and were treated with HC for 2 weeks. HQ-stimulated vitiligo in mice also produced melanocyte and melanosome degradation. The melanin content and tyrosinase activity of the mice (skin) that received the HC group significantly increased compared to the untreated and 8-methoxyprosalen (8-MOP) groups. These experiments suggest that the HC has potential protective and therapeutic effects for vitiligo.

Vitiligo is a type of chronic autoimmune skin disorder that is highly unpredictable. Houttuynia cordata Thunb. (HC) is a natural compound with several pharmacological properties; however, the fundamental mechanisms of HC effects on Vitiligo have yet to be fully understood. This study aimed to evaluate the effects of HC on the oxidative injury of melanocytes in vivo and in vitro. This study demonstrated that compounds significantly prevented the hydrogen peroxide (H2O2 )-induced B16F10 cell loss of viability and melanin synthesis; in addition, cell apoptosis-regulating of melanocytes significantly decreased, and the expression level of TRP-1 and MITF increased dose-dependently. In animal experiments, C57BL/6 mice received 5% hydroquinone (HQ) for 5 weeks and were treated with HC for 2 weeks. HQ-stimulated vitiligo in mice also produced melanocyte and melanosome degradation. The melanin content and tyrosinase activity of the mice (skin) that received the HC group significantly increased compared to the untreated and 8-methoxyprosalen (8-MOP) groups. These experiments suggest that the HC has potential protective and therapeutic effects for vitiligo.

Vitiligo is a type of chronic autoimmune skin disorder that is highly unpredictable. Houttuynia cordata Thunb. (HC) is a natural compound with several pharmacological properties; however, the fundamental mechanisms of HC effects on Vitiligo have yet to be fully understood. This study aimed to evaluate the effects of HC on the oxidative injury of melanocytes in vivo and in vitro. This study demonstrated that compounds significantly prevented the hydrogen peroxide (H2O2 )-induced B16F10 cell loss of viability and melanin synthesis; in addition, cell apoptosis-regulating of melanocytes significantly decreased, and the expression level of TRP-1 and MITF increased dose-dependently. In animal experiments, C57BL/6 mice received 5% hydroquinone (HQ) for 5 weeks and were treated with HC for 2 weeks. HQ-stimulated vitiligo in mice also produced melanocyte and melanosome degradation. The melanin content and tyrosinase activity of the mice (skin) that received the HC group significantly increased compared to the untreated and 8-methoxyprosalen (8-MOP) groups. These experiments suggest that the HC has potential protective and therapeutic effects for vitiligo.

Endochondral bone formation is the process by which mesenchymal cells condense into chondrocytes, which are ultimately responsible for new bone formation. The processes of chondrogenic differentiation and hypertrophy are critical for bone formation and are therefore highly regulated. The present study was designed to investigate the effect of aloe-emodin on chondrogenic differentiation in clonal mouse chondrogenic ATDC5 cells. Aloe-emodin treatment stimulated the accumulation of cartilage nodules in a dose-dependent manner. ATDC5 cells were treated with aloe-emodin and stained with alcian blue. Compared with the control cells, the ATDC5 cells showed more intense alcian blue staining. This finding suggested that aloe-emodin induced the synthesis of matrix proteoglycans and increased the activity of alkaline phosphatase. Aloe-emodin also enhanced the expressions of chondrogenic marker genes such as collagen II, collagen X, BSP and RunX2 in a time-dependent manner. Furthermore, examination of the MAPK signaling pathway showed that aloe-emodin increased the activation of extracellular signal-regulated kinase (ERK), but had no effect on p38 and c-jun N-terminal kinase (JNK). Aloe-emodin also enhanced the protein expression of BMP-2 in a time-dependent manner. Thus, these results showed that aloe-emodin exhibited chodromodulating effects via the BMP-2 or ERK signaling pathway. Aloe-emodin may have potential future applications for the treatment of growth disorders.
Alcian Blue ; Alkaline Phosphatase ; Animals ; Cartilage ; Chondrocytes ; Chondrogenesis ; Collagen ; Growth Disorders ; Hypertrophy ; JNK Mitogen-Activated Protein Kinases ; Mice ; Osteogenesis ; Phosphotransferases* ; Proteoglycans

Periodontal disease is primarily associated with bacterial infection such as dental plaque. Dental plaque, an oral biofilm harboring a complex microbial community, can cause various inflammatory reactions in periodontal tissue. In many cases, the local bacterial invasion and host-mediated immune responses lead to severe alveolar bone destruction. To date, plaque control, non-surgical, and surgical interventions have been the conventional periodontal treatment modalities. Although adjuvant therapies including antibiotics or supplements have accompanied these procedures, their usage has been limited by antibiotic resistance, as well as their partial effectiveness. Therefore, new strategies are needed to control local inflammation in the periodontium and host immune responses. In recent years, target molecules that modulate microbial signaling mechanisms, host inflammatory substances, and bone immune responses have received considerable attention by researchers. In this review, we introduce three approaches that suggest a way forward for the development of new treatments for periodontal disease; (1) quorum quenching using quorum sensing inhibitors, (2) inflammasome targeting, and (3) use of FDA-approved anabolic agents, including Teriparatide and sclerostin antibody.

Periodontal disease is primarily associated with bacterial infection such as dental plaque. Dental plaque, an oral biofilm harboring a complex microbial community, can cause various inflammatory reactions in periodontal tissue. In many cases, the local bacterial invasion and host-mediated immune responses lead to severe alveolar bone destruction. To date, plaque control, non-surgical, and surgical interventions have been the conventional periodontal treatment modalities. Although adjuvant therapies including antibiotics or supplements have accompanied these procedures, their usage has been limited by antibiotic resistance, as well as their partial effectiveness. Therefore, new strategies are needed to control local inflammation in the periodontium and host immune responses. In recent years, target molecules that modulate microbial signaling mechanisms, host inflammatory substances, and bone immune responses have received considerable attention by researchers. In this review, we introduce three approaches that suggest a way forward for the development of new treatments for periodontal disease; (1) quorum quenching using quorum sensing inhibitors, (2) inflammasome targeting, and (3) use of FDA-approved anabolic agents, including Teriparatide and sclerostin antibody.

Background: In lipopolysaccharide-induced RAW264.7 cells, Aster tartaric (AT) inhibits the nuclear factor kappa-light-chain-enhancer of activated B cells and MAPKs pathways and critical pathways of osteoclast development and bone resorption. Objectives: This study examined how aster saponin A2 (AS-A2) isolated from AT affects the processes and function of osteoclastogenesis induced by receptor activator of nuclear factor kappa-B ligand (RANKL) in RAW264.7 cells and bone marrow macrophages (BMMs). Methods: The cell viability, tartrate-resistant acid phosphatase staining, pit formation assay, polymerase chain reaction, and western blot were carried out to determine the effects of ASA2 on osteoclastogenesis. Results: In RAW264.7 and BMMs, AS-A2 decreased RANKL-initiated osteoclast differentiation in a concentration-dependent manner. In AS-A2-treated cells, the phosphorylation of ERK1/2, JNK, and p38 protein expression were reduced considerably compared to the control cells. In RAW264.7 cells, AS-A2 suppressed the RANKL-induced activation of osteoclast-related genes. During osteoclast differentiation, AS-A2 suppressed the transcriptional and translational expression of NFATc1 and c-Fos. AS-A2 inhibited osteoclast development, reducing the size of the bone resorption pit area. Conclusion AS-A2 isolated from AT appears to be a viable therapeutic therapy for osteolytic illnesses, such as osteoporosis, Paget’s disease, and osteogenesis imperfecta.

Osteoporosis is caused by an imbalance of osteoclasts and osteoblasts, and the major treatment technique for treating osteoporosis is to reduce the activity of osteoclastic bone resorption. Limonium tetragonum (LT) is a medicinal plant that contains bioactive molecules with anti-inflammatory and anti-cancer properties. Its effects on osteoclastogenesis, however, remain unclear.Limonium tetragonum extract (LTE) was examined for its inhibitory effect on osteoclastogenesis by TRAP and pit formation assay. As a result, LTE also significantly reduced TRAP formation, the capability to resorb calcium phosphate-coated plates, and F-actin ring formation.LTE reduced RANKL-induced activation of the MAPKs ERK, JNK, and p38 and the production of the transcription factors c-Fos and NFATc1 required for osteoclastogenesis. LTE also reduced the expression of osteoclastogenesis-related genes such as matrix metalloproteinase-9, tartrate-resistant acid phosphatase, and receptor activator of NF-κB. These findings suggest that LTE might be a promising treatment option for bone disorders caused by aberrant osteoclast production and function.