Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Myocutaneous Flap ; Pectoralis Muscles ; transplantation ; Ultrasonics

The effect of triptolide (TP) on the expression of receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG) was explored in rat adjuvant induced arthritis (AA). AA was induced in Wistar rats. Arthritis rats were treated with TP and methotrexate (MTX) at the onset (day 9) of arthritis. On the peak of arthritis (day 24), the expression of RANKL and OPG protein in the joints and RANKL mRNA in peripheral blood mononuclear cells (PBMC) was detected. TNF-alpha and IL-1beta levels in peripheral blood were determined. Bone erosion scores were also evaluated. The results showed that bone erosion scores in TP and MTX groups were lower than in AA group (P < 0.01); The expression levels of RANKL in the synovium (P < 0.01) and bone (P < 0.05), and OPG level in synovium (P < 0.05) were lower in TP group than in AA group (P < 0.05). In TP group, the expression levels of RANKL mRNA and TNF-alpha, IL-1beta in PBMC were lower than in AA group (all P < 0.01). It was concluded that TP could inhibit rat adjuvant arthritis bone erosion by suppressing the expression of RANKL.

Objective To explore the anti- inflammatory of pricking blood therapy in acute gouty arthritis rats. Methods 60 Sprague-Dawley rats were equally divided into normal group, bloodletting normal group, sham group, arthritis group, bloodletting group and ibuprofen group. The acute gouty arthritis model was established with injecting uric acid sodium salt into the right ankle joint cavity. The ibuprofen group was administrated with ibuprofen intragastrically, the bloodletting normal group and bloodletting group were pricked the right Kunlun (BL60) acupoint. The cross section diameter of the right ankle joint were measured before and after treatment. Levels of mRNA and protein of interleukin (IL)-10 and IL-4 expressed in ankle were determined with RT-PCR and Western blotting Results The cross section diameter increased in the bloodletting group compared with the normal group after treatment (P<0.05), and decreased (P<0.05) compared with the arthritis group and the ibuprofen group, while the expression of IL-10 mRNA increased (P<0.05) compared with the normal group, the arthritis group and the ibuprofen group, as well as the IL-10 protein compared with the normal group and the arthritis group (P< 0.05). The expression of IL-4 mRNA and protein increased without significance (P>0.05) in the bloodletting group compared with the normal group. Conclusion IL-10 may play a role of anti-inflammatory in pricking bloodletting therapy for acute gouty arthritis.

The effect of triptolide (TP) on the expression of receptor activator of nuclear factor-κB ligand (RANKL) and osteoprotegerin (OPG) was explored in rat adjuvant induced arthritis (AA).AA was induced in Wistar rats. Arthritis rats were treated with TP and methotrexate (MTX) at the onset (day 9) of arthritis. On the peak of arthritis (day 24), the expression of RANKL and OPG protein in the joints and RANKL mRNA in peripheral blood mononuclear cells (PBMC) was detected. TNF-α and IL-1β levels in peripheral blood were determined, Bone erosion scores were also evaluated. The results showed that bone erosion scores in TP and MTX groups were lower than in AA group (P＜0.01); The expression levels of RANKL in the synovium (P＜0.01) and bone (P＜0.05), and OPG level in synovium (P＜0. 05) were lower in TP group than in AA group (P ＜0.05). In TP group, the expression levels of RANKL mRNA and TNF-α, IL-1β in PBMC were lower than in AA group (all P＜0.01). It was concluded that TP could inhibit rat adjuvant arthritis bone erosion by suppressing the expression of RANKL.

Inflammation is involved in the development of various acute and chronic diseases in the body. Sustained inflammatory responses are key driving factors for diseases such as cancer， neurodegenerative diseases， cardiovascular diseases， metabolic syndrome， inflammatory bowel disease， and arthritis. Therefore， finding anti-inflammatory drugs is crucial for the prevention and treatment of various diseases. In recent years， there has been increasing attention to finding natural drugs with minimal toxic side effects. Lonicerae Japonicae Flos and Lonicerae Flos， as traditional Chinese medicines potent in clearing heat and removing toxins， have strong biological activity and multiple pharmacological effects. They are widely distributed in the plant world and have significant medicinal value. With the continuous advancement of the research on Lonicerae Japonicae Flos and Lonicerae Flos， they have been widely used in the medical field and possess great development potential. Currently， research mainly focuses on the anti-inflammatory mechanisms of Lonicerae Japonicae Flos and Lonicerae Flos， while systematic summaries of their anti-inflammatory active ingredients are rare. Therefore， this paper focuses on the differential analysis of the anti-inflammatory active components of Lonicerae Japonicae Flos and Lonicerae Flos. In addition， it reviewed the possible mechanisms by which extracts and active ingredients of Lonicerae Japonicae Flos and Lonicerae Flos may exert anti-inflammatory effects through various pathways， such as influencing the release of cellular inflammatory factors， regulating inflammatory signaling pathways such as nuclear factor-κB （NF-κB）， mitogen-activated protein kinase （MAPK）， signal transducer and activator of transcription 3 （STAT3）， MAPK/extracellular signal-regulated kinase （ERK）/c-Jun N-terminal kinase （JNK）， phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/NF-κB， and Janus kinase （JAK）/signal transducer and activator of transcription （STAT） signaling pathways， increasing antioxidant stress capacity， enhancing immune defense capabilities， and improving intestinal microbiota， aiming to provide a theoretical basis for the rational clinical application of Lonicerae Japonicae Flos and Lonicerae Flos.