Objective

2

To investigate the therapeutic effect of Lycopi Herba extract on chronic prostatitis （CNP） and explore the underlying action mechanism via the inflammasome NOD-like receptor protein 3 （NLRP3） pathway.

Method

2

Normal human prostatic stromal cells， namely WPMY-1 were induced by lipopolysaccharide （LPS） of 5 mg·L

-1

， and the effects of Lycopi Herba extract of 3.125， 6.25， 12.5， 25， 50， and 100 mg·L

-1

on interleukin-6 （IL-6） level released by LPS-induced WPMY-1 cells were detected by enzyme-linked immunosorbent assay （ELISA）. The half-maximal inhibitory concentration （IC

50

） was calculated. The expression of key proteins in the NLRP3 pathway was detected by western blot after Lycopi Herba

extract of 50， 75， and 100 mg·L

-1

was administered to WPMY-1 cells. The rat model of CNP was established by injecting carrageenan salt solution into the abdominal lobe of the prostate gland. Hematoxylin-eosin （HE） staining was used to observe the histopathological changes in the prostate gland in rats. The prostate organ index of rats was measured. The level of 5

α

-dihydrotestosterone （5

α

-DHT） in serum， as well as the levels of IL-6， tumor necrosis factor-

α

（TNF-

α

）， transforming growth factor-

β

1

（TGF-

β

1

）， cyclooxygenase-2 （COX-2）， prostaglandin E

2

（PGE

2

）， and inducible nitric oxide synthase （iNOS） in prostate tissue were detected by ELISA. The key protein expressions of COX-2， TGF-

β

1

， and NLRP3 pathway in prostate tissue were detected by Western blot. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the expressions of COX-2， IL-1

β

， TGF-

β

1

， and TNF-

α

mRNA in prostate tissue.

Result

2

Compared with the normal group， the level of IL-6 and the protein expression levels of NLRP3， ASC， Caspase-1， and IL-1

β

of WPMY-1 cells in the model group were increased （

P

<

0.05，

P

<

0.01）. Compared with the model group， Lycopi Herba

extract could inhibit the levels of IL-6 （

P

<

0.01） released by LPS-induced WPMY-1 cells， with IC

50

of 38.26 mg·L

-1

. The protein expression levels of NLRP3， ASC， and IL-1

β

in the low-， medium-， and high-dose groups of Lycopi Herba extract were significantly down-regulated （

P

<

0.05，

P

<

0.01）. The expression levels of Caspase-1 protein in medium- and high-dose groups of Lycopi Herba

extract were significantly down-regulated （

P

<

0.05，

P

<

0.01）. Compared with the sham operation group， the prostate organ index of rats in the model group was significantly increased （

P

<

0.01）， a large number of inflammatory cells were infiltrated in the prostate tissue， and the histopathological score was significantly increased （

P

<

0.05）； the levels of 5

α

-DHT in serum， the levels of TNF-

α

， PGE

2

， IL-6， TGF-

β

1

， NOS

2

/iNOS， and COX-2 in prostate tissue， and expression levels of COX-2， IL-1

β

， and TGF-

β

1

were significantly increased （

P

<

0.05，

P

<

0.01）. The mRNA expression levels of COX-2， TGF-

β

1

， NLRP3， Caspase-1， ASC， and IL-1

β

in prostate tissue were significantly up-regulated （

P

<

0.05，

P

<

0.01）. Compared with model group， the low and high doses of Lycopi Herba

extract could alleviate the pathological changes in prostate tissue induced by carrageenan， significantly reduce the level of 5

α

-DHT in serum， levels of TNF-

α

， PGE

2

， TGF-

β

1

， and iNOS in prostate tissue （

P

<

0.05，

P

<

0.01）， and mRNA expression levels of COX-2， IL-1

β

， and TGF-

β

1

（

P

<

0.05，

P

<

0.01）. The protein expression levels of COX-2， Caspase-1， ASC， and NLRP3 in prostate tissue were significantly down-regulated （

P

<

0.05，

P

<

0.01）. The prostate organ index of the low-dose group of Lycopi Herba

extract was significantly decreased （

P

<

0.01）. The level of COX-2 in prostate tissue of the high-dose group of Lycopi Herba

extract was significantly decreased， and the protein expression levels of TGF-

β

1

and IL-1

β

were significantly down-regulated （

P

<

0.05）.

Conclusion

2

Lycopi Herba extract has an obvious therapeutic effect on CNP and may reduce inflammation by inhibiting the activation of the inflammasome NLRP3 signaling pathway.