Objective To explore the protective effects of lycium barbarum polysaccharides(LBP) on fibroblast in vitro irradiated by ultraviolet A(UVA). Methods Taking the primary cultured fibroblast as objects, the fibroblast was irradiated by UVA ( irradiation intensity: 2.4 J/cm2). The fibroblast was randomly divided into six groups, control group, UVA radiated group and four protective groups(0.1 mg/ml LBP, 0.2 mg/ml LBP, 0.4 mg/ml LBP and 0.8 mg/ml LBP). The activities of cell proliferation were measured by MTT methods. The contents of MDA, the activities of SOD in the fibroblasts, and the activities of LDH in the supernatants of fibroblasts were determined by biochemical methods. Results The fibroblasts were irradiated by UVA (irradiation intensity: 2.4 J/cm2),the activities of cell proliferation was decreased,the activities of SOD was decreased too, the content of MDA and LDH increased. Compared with UVA irradiated group,in the given concentration,LBP could improve the activities of cell’s proliferation,improve the activities of SOD and decrease the contents of MDA in the cell, and decrease the content of LDH in the supernatants of cells significantly (P

0.05).DBP and DEHP obviously induced a decrease in organ body weight ratios of testis and epididymis and an increase in organ body weights ratios of liver.Obvious decrease in the sperm counts,spermatozoon survival rate and significant increase in the rate of the sperm deformation were observed.There was synergism between DBP and DEHP on the testis,epididymis and liver organ body weight ratio,as well as sperm counts,sperm survival and deformation rates.Pathological examination showed the seminiferous tubules were irregular shape,degenerative atrophy and interstitial substance broadening,and the seminiferous epithelium were degeneration.Epididymis epithelium was damaged and few of mature sperm was seen.Conclusion DBP combined with DEHP can cause obvious toxic effects on reproductive function in male rats.DBP and DEHP mixture can strongly affect the sperm quantity and quality.Also,some toxic effects to epididymis are observed.

Objective To study the combined toxic effects of di-n-butyl phthalate(DBP)and di-2-ethylhexyl phthalate(DEHP)on sex hormone and lipid peroxidation in male rats.Methods According to 2?2 factorial analysis,thirty-two healthy and clean adult male SD rats were randomly divided into 4 groups,including a control group(given coin oil) and three experimental groups:DBP(1/20 LD50,1.0 g/kg,dissolved in coin oil),DEHP(1/20 LD50,1.7 g/kg,dissolved in coin oil) and DBP+DEHP(1.0 g/kg + 1.7 g/kg,dissolved in coin oil),8 rats in each group,through gavage,once a day,for 8 consecutive weeks.The spectrophotometric method was used to measure the activity of lipid peroxidation SOD,GSH and GSH-Px level in testis homogenate.The activities of ACP,AKP and ?-GT were assessed in testis homogenate.Radioimmunoassay was used to determine the testosterone,LH and FSH levels in the serum.Results There was synergism between DBP and DEHP on the SOD activity in testicle and testosterone level in serum,and there was antagonism between DBP and DEHP on the ?-GT and ACP activity in testicle,as well as the FSH level in serum.Conclusion DBP combined with DEHP can cause obvious toxic effects on reproductive function in male rats.The change of testosterone biosynthetic enzymes and the levels of T in serum and disordered physiologic balances of hypothalamic-pituitarytestis axis may be key factors contributing to the decrease of testosterone,then the decrease of reproductive function in male rats.

Pathological vascular remodeling is a hallmark of various vascular diseases. Previous research has established the significance of andrographolide in maintaining gastric vascular homeostasis and its pivotal role in modulating endothelial barrier dysfunction, which leads to pathological vascular remodeling. Potassium dehydroandrographolide succinate (PDA), a derivative of andrographolide, has been clinically utilized in the treatment of inflammatory diseases precipitated by viral infections. This study investigates the potential of PDA in regulating pathological vascular remodeling. The effect of PDA on vascular remodeling was assessed through the complete ligation of the carotid artery in C57BL/6 mice. Experimental approaches, including rat aortic primary smooth muscle cell culture, flow cytometry, bromodeoxyuridine (BrdU) incorporation assay, Boyden chamber cell migration assay, spheroid sprouting assay, and Matrigel-based tube formation assay, were employed to evaluate the influence of PDA on the proliferation and motility of smooth muscle cells (SMCs). Molecular docking simulations and co-immunoprecipitation assays were conducted to examine protein interactions. The results revealed that PDA exacerbates vascular injury-induced pathological remodeling, as evidenced by enhanced neointima formation. PDA treatment significantly increased the proliferation and migration of SMCs. Further mechanistic studies disclosed that PDA upregulated myeloid differentiation factor 88 (MyD88) expression in SMCs and interacted with T-cadherin (CDH13). This interaction augmented proliferation, migration, and extracellular matrix deposition, culminating in pathological vascular remodeling. Our findings underscore the critical role of PDA in the regulation of pathological vascular remodeling, mediated through the MyD88/CDH13 signaling pathway.
Mice ; Rats ; Animals ; Myeloid Differentiation Factor 88/metabolism* ; Vascular Remodeling ; Cell Proliferation ; Vascular System Injuries/pathology* ; Carotid Artery Injuries/pathology* ; Molecular Docking Simulation ; Muscle, Smooth, Vascular ; Cell Movement ; Mice, Inbred C57BL ; Signal Transduction ; Succinates/pharmacology* ; Potassium/pharmacology* ; Cells, Cultured ; Diterpenes ; Cadherins