Objective To observe the effect of Manzhi Kechuan Ling(MKL)on pulmonary function and quality of life (QOL)of patients with chronic obstructive pulmonary disease (COPD)at stationary stage.Methods Seventy-six COPD patients were randomized into two groups.The treatment group (N=40)received oral use of MKL (mainly composed of Radix Ginseng,Radix Astragali,Rhizoma Atractylodis Macrocephalae,Colla Cornus Cervi,Placenta Hominis,Gecko,Semen Juglandis,Gecko,Fructus Perillae,Bulbus Fritillariae Cirrhosae,Rhizoma Pinelliae)for 6 months,and was followed up for another 6 months after suspension of medication.The control group (N=36)did not receive any medication.The pulmonary function,TCM syndrome scores,QOL scores and annual acute attack times were examined before treatment,6 and 12 months after treatment.Meanwhile,artery blood gas analysis was performed before treatment and 6 months after treatment.Results Inthe treatment group,the pulmonary function indexes of forced expiratory volume in one second (FEV1)andforced vital capacity (FVC)were improved 6 months after treatment (P0.05).In the control group,FEV1 and FVC presented a decreasing trend 6 and 12 months after treatment,and FEV1 and FCV 12 months after treatment differed from those before treatment (P0.05).There showed statistical differences of PaO2 and PaCO2 between the two groups 6 months after treatment(P

BACKGROUND: A variety of antioxidants exhibit anti-arthritis effects by inhibiting the production of inflammatory factors. Pterostilbene is a powerful natural antioxidant; however, there is no report on its effect against oxidative stress in chondrocytes. OBJECTIVE: To investigate the effect of pterostilbene on oxidative stress induced apoptosis in human chondrocytes METHODS: Normal human articular chondrocytes were cultured in medium containing different concentrations of pterostilbene (7.8-32 000 μg/L) for 24 continuous hours to determine the optimal concentration of pterostilbene. Normal human articular chondrocytes cultured in vitro were randomized into control group, pterostilbene group (treatment with 125 μg/L pterostilbene), hydrogen p eroxide (H2O2) group (treatment with 0.2 mmol/L H2O2), and H2O2 plus pterostilbene group (pretreatment with 125 μg/L pterostilbene followed by continuous treatment in the medium containing 125 μg/L pterostilbene and 0.2 mmol/L H2O2). After treating for 24 hours, the cell proliferation rate was detected by MTT experiment, the cell morphology and number by hematoxylin-eosin staining, the cell activity was measured by FDA/PI staining, and the changes of proteoglycan content were observed by saffron O staining. The expression of chondrogenesis marker genes aggrecan and type II collagenase 1 was detected by RT-PCR. An approval for the study protocol was validated by the Ethic Committee of the First Affiliated Hospital of Guangxi Medical University with an approval No. 20180500 8. RESULTS AND CONCLUSION: The results of MTT assay showed that pterostilbene could significantly promote chondrocyte growth at 15.6-250 μg/L, especially at 125 μg/L. The results of hematoxylin-eosin staining and FDA/PI staining further showed that pterostilbene could inhibit H2O2-induced chondrocyte apoptosis, promote chondrocyte proliferation, and increase cell viability. The results of saffron O staining showed that pterostilbene promoted the secretion of proteoglycan by chondrocytes and inhibited the adverse effects of H2O2 on chondrocytes. The results of RT-PCR further revealed that pterostilbene could promote the expression of aggrecan and type II collagenase 1 genes in chondrocytes damaged by oxidative stress and improve the chondrocyte differentiation function. In conclusion, pterostilbene can promote chondrocyte proliferation and inhibit human articular chondrocyte apoptosis caused by oxidative stress.

BACKGROUND:The mechanism of steroid-induced avascular necrosis of the femoral head is stil unclear, Cx43 protein as the main gap junction in bone tissue, through transmitting information between osteoblasts, regulates bone cel growth and differentiation, compensatory bone increase or decrease. The relationship between Cx43 protein and steroid-induced avascular necrosis of the femoral head is stil rarely reported.
OBJECTIVE:To explore the changes in Cx43 expression in rabbit models of steroid-induced vascular necrosis of the femoral head.
METHODS:Forty New Zealand rabbits were equal y and randomly divided into model group and control group. Rabbits in the model group were used to establish models of steroid-induced avascular necrosis of the femoral head using endotoxin and hormone. Rabbits in the control group were injected with the same volume of physiological saline at the same time points.
RESULTS AND CONCLUSION:At 4 weeks after model establishment, hematoxylin-eosin staining results revealed that in the model group, the trabecula became thin and distributed disorderly in the femoral subchondral area. Empty lacuna increased significantly. Adipocytes increased. Hematopoietic cel s in medul ary cavity apparently diminished. In the control group, trabecula arranged orderly and empty lacuna could be seen. Bone marrow cel s were abundant, but adipocytes were less. Immunohistochemical method demonstrated that Cx43 protein expression was observed in osteoblasts of the edge of trabecula, cytoplasm of osteoblasts of trabecula, and bone marrow stromal cel s. Western blot assay results showed that alkaline phosphatase and Cx43 protein expression was lower in the model group than in the control group (P<0.05). Results indicated that Cx43 protein expression decreased in the model rabbits, which may be the key link of the occurrence and development of steroid-induced avascular necrosis of the femoral head.