Zhuling Decoction

This study aimed to determine whether Dahl salt‐sensitive rats fed a high‐salt diet would show features of nocturia due to nocturnal polyuria and to examine the efficacy of choreito (CRT) on nocturnal polyuria.

Dahl salt‐sensitive rats were divided into three groups. Group A was fed a 4% salt diet, group B a 2% salt diet, and group C a normal 0.3% salt diet. In groups α and β, other rats were further divided into two groups: The rats in group α were fed a 2% salt plus 3% CRT diet, and those in group β, were fed a 2% salt diet. Each rat was placed in an individual metabolic cage for 24 hours every week for 6 weeks. Water intake, urine production, voiding frequency, and voided volume per micturition were recorded.

The systolic blood pressure increased in the group fed a 4% salt diet compared to groups fed with a 2% and 0.3% salt diet. The urinary volume was higher in the groups fed with 4% and 2% salt than in the group fed with 0.3% salt. Further, water intake in the group fed a 2% salt plus 3% CRT diet was significantly lower than that in the group fed with a 2% salt diet.

Dahl salt‐sensitive rats fed a 2% salt diet were candidates for a model of nocturnal polyuria. Using this model, we suggest that CRT reduces water intake in the active phase and contributes to water restriction in the treatment of nocturnal polyuria.

We previously revealed that Choreito, a traditional Kampo medicine, strongly inhibits bladder carcinogenesis promotion. We have also shown that Polyporus sclerotium, which is one of the crude drugs in Choreito, has the strongest bladder carcinogenesis inhibitory effect and that the ergosterol contained in Polyporus sclerotium is the main active component. In this study, we analyzed the mechanism by which ergosterol inhibits bladder carcinogenesis. Rats were given an N-butyl-N-(4-hydroxybutyl) nitrosamine (BHBN) solution ad libitum, and then a promoter [saccharin sodium (SS), DL-tryptophan, or BHBN] was administered together with ergosterol or its metabolite, brassicasterol. The bladders were removed from rats, and the inhibitory effect on carcinogenesis promotion was evaluated by an agglutination assay with concanavalin A (Con A). Although the oral administration of ergosterol inhibited the promotion of bladder carcinogenesis with SS, the intraperitoneal administration of brassicasterol showed a stronger effect. The effect of brassicasterol on carcinogenesis promotion was observed regardless of the type of promoter. Administration of testosterone to castrated rats increased the number of cell aggregates caused by Con A. In contrast, intraperitoneal administration of brassicasterol to castrated rats treated with testosterone significantly decreased the number of cell aggregates, confirming the inhibition of bladder carcinogenesis promotion. The inhibitory effect of ergosterol on bladder carcinogenesis is due to brassicasterol, a metabolite of ergosterol. The action of brassicasterol via androgen signaling may play a role in the inhibitory effect on bladder carcinogenesis promotion.