RESUMO
Objective: To study the influence of total salvianolic acid(TSA) on the renal interstitial fibrosis caused by unilateral ureteral obstruction (UUO) in rats. Methods: Forty healthy Sprague-Dawley rats were randomly divided into 4 groups: the UUO group, sham operation group, angiotensin-converting enzyme inhibitor ( ACEI)-treated group (positive control), and TSA-treated group. The rats in UUO group and sham-operation group received gastric gavage with normal saline for 8 days before operation; rats in ACEI-treated group and TSA-treated group received ACEI (6 mg/kg by daily gastric gavage for 8 days) and TSA (20 mg/kg by daily gastric gavage for 8 days), respectively. All rats were killed 7 days after operation and the expression of transforming growth factor-β 1 (TGF-β1) was detected by immunohistochemical method. The dynamic histological changes of renal interstitial tissues were observed by H-E and Masson staining. Results: TGF-β1 expression in TSA-treated (1.38 ± 0.26) and ACEI-treated (1.38 ± 0.26) groups was significantly lower than that in UUO group (P < 0.05). TSA obviously reduced TGF-β1 expression and collagen deposition in the renal interstitial tissues and improved the renal pathological changes in UUO rats. Conclusion: TSA can evidently inhibit UUO-induced renal interstitial fibros is in rats, which might be related with the down regulation of TGF-β1 expression.
RESUMO
Objective: To study the inhibition of xanthine oxidase by renierol extracted from South China Sea sponge and study the influence of renierol on hyperuricemia in mice. Methods: After extracted from South China Sea sponge, renierol (20, 40, 60 μg/ml) was added to a system containing xanthine oxidase (0. 1 μ/ml) and xanthine (50 μmol/ml); allopurinol (1 μg/ml) was also addded to the system as positive control. The 5 min-fomation of superoxide anions was used to determine the activity of xanthine oxidase (Nitro Blue Btetrazolium reduction). Renierol (20, 40, 60 μg/ml) was added to 25°C pre-heated pyrogallol autoxidation to observe its eliminating effect on free radicals through determining the absorbance rate at 420 nm wavelength. Potassium oxonate, a uricase inhibitor, was used to induce hyperuricemia in mice and the mice were then treated with oral renierol (10, 20, 30 mg · kg-1) or allopurinol (2 mg/kg) as positive control. The decrease of serum uric acid induced by renierol was determined by automatic biochemical analyzer. Results: Renierol was demonstrated to be a competitive inhibitor of xanthine oxidase in vitro , with its IC50 value being 1.36 μg · ml-1. It also decreased uric acid in vivo. Conclusion: Renierol can decrease serum uric acid through inhibiting the xanthine oxidase.
RESUMO
Objective: To study the inhibitory effect of rosmarinic acid on xanthine oxidase. Methods: Xanthine oxidase (0.1 U/ml) was incubated with xanthine (1 mmol/L for determining formation of uric acid; 50 μmol/L for determining superoxide anions) in the presence of 20, 40 and 60 μg/ml rosmarinic acid or allopurinol as positive control. The formation of uric acid was determined by automatic biochemical analyzer 5 min after reaction and the production of superoxide anions was measured by Nitro Blue Btetrazolium (NBT) reduction. HL-60 cells (1 ml, 2×105/ml) were pretreated with xanthine (100 μl, 6 mol/L) and xanthine oxidase (100 μl, 0.1 U/ml), then rosmarinic acid (500 μg/ml) or allopurinol (1 μg/ ml, as positive control) (Annexin V-PI kit) was added to determine the cell apoptosis rate. HL-60 cells (1 ml, 2×105/ml) were also pretreated with xanthine (100 μl, 6 mol/L) and xanthine oxidase (100 μl, 0.1 U/ml), then rosmarinic acid (500 μg/ml) or SOD (100 U/ml, as positive control) (cell cycle method) was added to determine the cell apoptosis rate. Results: Rosmarinic acid obviously inhibited the production of uric acid and superoxide anion-induced reaction in NBT assay, with their IC50 being 56 μg/ml and 21 μg/ml, respectively. The rates of apoptosis inhibition by rosmarinic acid were both over 40% by Annexin V-PI kit and cell cycle method. Conclusion: Rosmarinic acid is a competitive inhibitor of xanthine oxidase.