Objective To observe whether hydrogen sulfide modulates adipocytes to secrete adiponectin.Methods Thirty-two male SD rats were randomly divided into normal diet group (n =8),high-fat diet group (n =8),high-fat + cysteine group (n =8),and high-fat + propargylglycine (cystathionine-γ-lyase inhibitor) group (n =8).The fatty liver animal model was established using the high fat diet; meanwhile,L-cysteine was applied to the animals to produce endogenous hydrogen sulfide and propargylglycine to inhibit the production of endogenous hydrogen sulfide.Fatty degeneration of the hver of animals and plasma within the adiponectin concentration was observed after 8 weeks.The omental adipose tissues were excluded and digested using collagenase Ⅰ to isolate fat cells.Sodium hydrosulfide and propargylglycine was applied to stimulate the cells in vitro for 7 days before the detection of the cell supernatant adiponectin content.Results Liver steatosis was established after highfat diet for eight weeks.Steatosis was significantly extenuated after the application of L-cysteine and aggravated by propargylglycine.Plasma hydrogen sulfide and adiponectin levels in fat diet group animals were (21.13 ± 7.06) mmol/L and (3.16 ± 1.15) mg/L respectively,which significantly decreased when compared with the normal diet group with the levels of hydrogen sulfide (29.13 ± 13.06) mmol/L and adiponectin (8.98 ± 2.84) mg/L (P=0.0229,P=0.0062).Hydrogen sulfide [(35.47 ±9.04) mmol/L] and adiponectin [(6.54 ± 1.38) mg/L] levels in the high fat + cysteine group significantly increased (P =0.0032,P =0.0131).However,hydrogen sulfide [(16.65 ±8.79) mmol/L] and adiponectin [(2.50±0.91) mg/L] in high fat + propargylglycine group were significantly decreased (P =0.0191,P =0.0021).Hydrogen sulfide was not significantly differem in the supematam of adipocyte isolated from normal diet group [(26.77 ± 12.65) mmol/L] and from high-fat diet group [(28.76 ±9.09) mmol/L] (P =0.0927),but that in the sodium hydrosulfide and propargylglycine ceils supematants significandy either increased or decreased (P =0.0000,P =0.0000).Adiponectin in the supematants of high-fat diet group and normal diet group adipocyte showed no significant difference [(4.21 ± 1.61) mg/L vs (4.49 ± 1.09) mg/L,P =0.1076)].The levels of adiponectin in sodium hydrosulfide and propargylglycine cell supernatants increased and decreased respectively than that in higher fat diet group cells [(5.77 ±0.86) mg/L vs (4.21 ±1.61) mg/L,P =0.0094; (3.01 ±1.26) mg/L vs (4.21 ± 1.61) mg/L,P =0.0108].Conclusion Hydrogen sulfide promotes adipocytes to secrete adiponectin.

Objective To investigate the effects of parathyroid hormone (PTH) on the synthesis and secretion of collagen Ⅲ and fibronectin (FN), and the expressions of plasminogen activator inhibitor-1 (PAI-1), matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA in cultured human renal tubular epithelial cells (HK-2).Methods HK-2 cells were cultured in DMEM-F12 medium supplemented with 5% FBS. Cells were exposed to different concentrations of PTH (0, 10-12, 10-11, 10-10, 10-9, 10-8 mol/L) for 48 h, or 10-8 mol/L PTH at different time (0, 12, 24, 48, 72 h). The gene expressions of collagen Ⅲ,FN, PAI-1, MMP-1, and TIMP-1 were detected by semi-quantitative RT-PCR. The protein expression of collagen Ⅲ was detected by Western blotting. The level of FN in the supernatant was assayed by enzyme linked immunosorbent assay (ELISA). Results PTH increased gene expressions of collagen Ⅲ, FN, PAI-1 and TIMP-1 in a dose- and time-dependent manner, but decreased MMP-1 gene expression. Then the ratio of MMP-1/TIMP-1 was decreased. PTH increased the collagen Ⅲ protein expression in cultured HK-2 cells and the level of FN in the supernatant of cultured HK-2 cells in a dose- and time-dependent manner. Conclusion PTH can up-regulate PAI-1, TIMP-1 gene expressions, and down-regulate MMP-1 gene expression,resulting in elevation of extracellular matrix (ECM) synthesis and reductim of degradation.

OBJECTIVETo verify the clinical efficacy on postmenopausal osteoporosis treated with acupoint injection of salmon calcitonin.

METHODSNinety patients of postmenopausal osteoporosis were randomized into three groups, 30 cases in each one. In the acupoint injection group, Shenshu (BL 23) and Zusanli (ST 36) were selected bilaterally. The injection 4 mL was prepared with salmon calcitonin 100 U (1 mL) and 0.9% sodium chloride injection. Each acupoint was stimulated with the injection, 1 mL. In the blank group, 0.9% sodium chloride injection was applied to bilateral Shenshu (BL 23) and Zusanli (ST 36), 1 mL at each acupoint. In the intramuscular injection group, salmon calcitonin 100 U was injected at gluteus maximus. The treatment was given once every two days in the patients of the three groups and lasted for 2 months. The levels of bone mineral density (BMD), bone alkaline phosphatase (NBAP), C-terminal telopeptides of typeⅠcollagen (CTX), urine calcium/creatinine (Ca/Cr) and the symptom score of osteoporosis were detected in the patients of the three groups before and after treatment.

RESULTSIn the patients of the three groups, NBAP and BMD in lumbar vertebra after treatment were higher than those before treatment (all<0.05); CTX, Ca/Cr and symptom score were lower than those before treatment (all<0.05). After treatment, NBAP was (32.7±2.5) μg/L in the acupoint injection group, higher than those in the blank group and the intramuscular injection group (both<0.05). In the acupoint injection group, CTX was reduced to (239.7±63.6) μmmol/L and Ca/Cr was reduced to 0.525±0.274, apparently lower than those in the blank group and intramuscular injection group (both<0.05). After treatment, in the acupoint injection group, BMD of lumbar vertebra was (0.731±0.062) g/m, higher than the level of the rest two groups (both<0.05). After treatment, the symptom score was 5.2±0.6 in the acupoint injection group, lower than those in the blank group and intramuscular injection group (both<0.05).

CONCLUSIONSSalmon calcitonin injec-tion at Zusanli (ST 36) and Shenshu (BL 23) achieves significant efficacy on postmenopausal osteoporosis, stimulating osteoblast activity and inhibiting bone absorption of osteoclast.