To observe the effect of Qianliening(QLN) on collagens Ⅱ,Ⅲ,and Ⅳ mediated by matrix metalloproteinase-2(MMP-2) and tissue inhibitor of metalloproteinase-2(TIMP-2) and its mechanism in treating benign prostatic hyperplasia(BPH).Methods:Sprague-Dawley(SD) rats were divided into a blank group,model group,low-dose QLN group,medium-dose QLN group,high-dose QLN group,and model group.The BPH model was established in each dose group of QLN,and the treatment group was treated with QLN by gavage.After four weeks of treatment,the weight and volume of the prostate were measured; the prostate index was calculated,and the protein expressions of collagens Ⅱ,Ⅲ,and Ⅳ were observed by immunohistochemistry.Human prostatic hyperplasia cells(BPH-1) were cultured and divided into a blank group(control group,0 mg/mL),low-dose QLN group(0.25 mg/mL),medium-dose QLN group(0.5 mg/mL),and high-dose QLN group(1 mg/mL).Cell morphology was observed by an inverted microscope.The cell viability was detected by cell counting Kit-8(CCK-8) assay.The protein expressions of MMP2,TIMP-2,and collagens Ⅱ,Ⅲ,and Ⅳ were detected by Western Blot.Results:Compared with the model group,the prostate weight,volume,and index of rats in the QLN groups were significantly reduced(P<0.05),and the protein expression of collagens Ⅱ,Ⅲ,and Ⅳ was significantly reduced by(P<0.05).Cell experiment showed that the density of BPH-1 cells in the medium-dose QLN group and high-dose QLN group was significantly reduced,and the cell growth rate was slow.The results of CCK8 showed that the viability of BPH-1 cells in the medium-dose QLN group and high-dose QLN group within 24 hours and 48 hours was significantly reduced(P<0.05).Western Blot showed that the protein expression of MMP-2 and collagens Ⅱ,Ⅲ,and Ⅳ decreased significantly,while TIMP-2 protein expression increased significantly.Compared with the blank group,the difference was statistically significant(P<0.05).Conclusion:QLN can effectively degrade the expression of Collagen Ⅱ,Ⅲ,and Ⅳin prostate tissue of rats with BPH,and it has an obvious inhibitory effect on BPH-1 cells.Its therapeutic mechanism may be related to regulating the MMP-2 and TIMP-2 to degrade collagens Ⅱ,Ⅲ,and Ⅳ,so as to treat BPH.