Intervention of Bazi Bushen Capsule on Benign Prostatic Hyperplasia Concomitant with Erectile Dysfunction Induced by Testosterone Supplementation in Spontaneously Hypertensive Rats

A Chinese herbal capsule eased both prostate enlargement and erectile dysfunction in rats—finasteride only fixed one

Journal: Chinese Journal of Integrative Medicine | Published: 2025-05-27 | Type: Journal Article | PMID: 40419843 Authors: Zhang Run-Tao, Hou Yun-Long, Li Meng-Nan, et al. (Hebei Medical University; State Key Laboratory for Innovation and Transformation of Luobing Theory; Nanjing University of Chinese Medicine; Hebei University of Chinese Medicine) Funding/COI: Funding source not listed in the paper. Authors declare no conflicts of interest.

Summary

Researchers gave testosterone injections to hypertensive rats to induce both prostate enlargement and erectile dysfunction simultaneously, then treated them with a traditional Chinese medicine capsule called Bazi Bushen (BZBS) at two doses, comparing it against finasteride, a standard BPH drug. BZBS reduced prostate size and inflammation similarly to finasteride, but unlike finasteride, it also improved markers of erectile tissue health—smooth muscle content, blood vessel signaling molecules, and fibrosis. The authors' conclusion is that inflammation drives both conditions and that BZBS works by damping inflammatory pathways in both tissues at once.

Claims

• BZBS reduced prostate wet weight and prostate index compared to the untreated testosterone-injected group (P<0.01)
• BZBS altered expression of proliferation and apoptosis markers (PCNA, Bax, Bcl-2) in prostate tissue (P<0.05 or P<0.01)
• BZBS reduced corpus cavernosum fibrosis and increased smooth muscle area, alongside upregulated α-smooth muscle actin (P<0.05 or P<0.01)
• BZBS increased RhoA/ROCK2, eNOS, nitric oxide, and cGMP—signaling molecules involved in erectile function (P<0.05 or P<0.01)
• BZBS lowered dihydrotestosterone and 5α-reductase type II, and reduced PSA levels (P<0.05 or P<0.01)
• BZBS reduced inflammatory markers in both prostate and corpus cavernosum tissue, whereas finasteride reduced inflammation only in the prostate
• Network pharmacology analysis identified multiple inflammation-related targets as the proposed mechanism

Study Quality

This is a controlled animal experiment with five groups of 10 rats each (50 total): a normal-strain control (Wistar-Kyoto rats), a testosterone-only model group, two BZBS dose groups, and a finasteride comparator, randomized by "random number table." The 28-day design and inclusion of an active comparator (finasteride) is a reasonable structure for a mechanistic rodent study, and pairing tissue-level biochemistry with network pharmacology gives some mechanistic triangulation rather than resting on a single readout.

That said, n=10 per group is small even by rodent-study standards, and the paper reports a large volume of biochemical endpoints (androgen markers, apoptosis markers, fibrosis markers, inflammatory markers, signaling molecules) without describing correction for multiple comparisons. Spontaneously hypertensive rats are a specific hypertension model, not a validated standard for isolated BPH/ED research, and testosterone-induced BPH+ED in this strain is a proxy model whose relevance to human disease—where BPH and ED arise from aging, vascular disease, and hormonal changes over decades rather than a 28-day androgen bolus—is unestablished.

Red Flags

• No funding source disclosed at all, which is unusual for a study using network pharmacology and extensive lab assays—typically grant-supported work
• Small group sizes (n=10) for a study measuring dozens of biochemical endpoints
• No mention of blinding for pathology scoring or biochemical assays
• Proprietary herbal formulation (BZBS) with no breakdown of active constituents or dose-response data beyond "low" and "high"
• Testosterone-induced rat model is an artificial proxy for a disease process that in humans is chronic and multifactorial
• No behavioral or functional erectile measurements (e.g., intracavernosal pressure)—only tissue-level biochemical and structural markers, so "improved ED" is inferred, not directly measured

Strengths

• Includes both a healthy strain control and an active-drug comparator (finasteride), allowing relative rather than just placebo comparison
• Combines histology, biochemistry, and network pharmacology instead of a single outcome measure
• Explicitly disclosed no conflicts of interest
• Reports specific P-values and directional effects across multiple pathways rather than vague summary language

Verdict

This is a preliminary rodent mechanistic study, not evidence that this capsule does anything for human BPH or ED—there's no dosing translation, no functional erectile measurement, and no disclosed funding for a fairly resource-intensive multi-assay design. The inflammation angle linking BPH and ED is a legitimate research question, but the small sample size, proxy disease model, and absence of hard functional endpoints mean this belongs in the "hypothesis-generating" bin, several steps removed from anything clinically actionable.