*2.3. Urinary Protein Excretion*

Proteinuria is the most important feature of nephrotic syndrome. To measure the urinary protein levels, the rats were placed in individual metabolic cages for 24 h urine collection once a week. We detected the 24 h urinary protein excretion of all rats. As shown in Table 4, two weeks after adriamycin administration (0 week in Table 4, the beginning time of drug administration), the 24 h urinary protein of the model group was significantly higher than that of the normal group and became higher over time. This phenomenon proved that adriamycin treatment can be used to form a rat model of nephropathy with continuous aggravation, which is similar to nephrotic syndrome. The urinary protein excretion of rats treated with fucoidan or LMWF (50 or 100 mg/kg) was significantly reduced after administration, which was significantly different from that of the model rats. The results

suggested that both fucoidan and LMWF could ameliorate the symptoms of hyperalbuminuria and gradually recover the damage of glomerular filtration membrane caused by adriamycin. Compared with fucoidan, LMWF at dose of 100 mg/kg had a much lower urinary protein excretion (*p* < 0.05, three weeks after drug administration), suggesting that low-molecular-weight fucoidan could inhibit the production of proteinuria with a higher activity.


**Table 4.** Effect of fucoidan and LMWF treatment on 24 h urinary protein of rats (*X* ± *S*, mg/mL).

: *p* < 0.05, : *p* < 0.01 (vs normal group); \*: *p* < 0.05, \*\*: *p* < 0.01 (vs model group).
