: Berberine (BBR) is a botanic alkaloid extracted from Coptis chinensis (Huanglian), which has various properties, compassing anti-hyperglycemia, anti-obesity, anti-inflammation, and improve insulin resistance, etc. Several researches have confirmed that BBR has effective actions in treating glycolipid metabolic abnormalities. BBR also has beneficial in regulating intestinal flora. Metabolic diseases are strongly associated with metabolic disorders, which are growing in the population and dramatically impacting human health, which also have been considered as a leading cause of diseases and death globally. This review is to evaluate the metabolic properties of BBR, and its potential application to the treatment of metabolic diseases by its effective actions on metabolic disorders.

Previous studies observed have reported that electroacupuncture (EA) is effective in relieving diabetic bladder dysfunction (DBD); however, little is known about the mechanism. Therefore, we explored the effects and mechanisms of EA on DBD in streptozotocin–high-fat diet- (STZ–HFD-) induced diabetic rats. The Sprague-Dawley male rats were divided randomly into four groups: normal group, diabetes mellitus group (DM group), DM with EA treatment group (EA group), and DM with sham EA treatment group (sham EA group). After 8 weeks of EA treatment, the body weight, serum glucose, bladder weight, and cystometrogram were evaluated. The bladder wall thickness was examined by abdominal ultrasound imaging. After the transabdominal ultrasound measurements, hematoxylin-eosin (HE) staining was used to observe the bladder mucosa layer. The bladder detrusor smooth muscle cells (SMCs) and fibroblasts were observed under transmission electron microscopy (TEM). The phospho-myosin light chain (p-MLC), phospho-myosin light chain kinase (p-MLCK), and phospho-myosin phosphatase target subunit 1 (p-MYPT1) levels in the bladder were examined using Western blot. The bladder weight, serum glucose, bladder wall thickness, volume threshold for micturition, and postvoid residual (PVR) volume in the diabetic rats were significantly higher than those in the control animals. EA treatment significantly reduced the bladder weight, bladder wall thickness, volume threshold for micturition, and PVR volume in diabetic rats. EA caused a significant increase in the MLC dephosphorylation and MLCK phosphorylation levels in the group compared to the sham EA and model groups. EA reduced the infiltration of inflammatory cells in the bladder mucosa layer of diabetic rats. In addition, EA repaired the damaged bladder detrusor muscle of diabetic rats by reducing mitochondrial damage of the SMCs and fibroblasts. Therefore, EA could reduce the bladder hypertrophy to ameliorate DBD by reversing the impairment in the mucosa layer and detrusor SMCs, which might be mainly mediated by the regulation of p-MLC and p-MLCK levels.

Author contributions: X.Z. contributed significantly to analysis and manuscript preparation. Q.H.D. conceived and designed the exper-iments. J.H.D. analyzed the data. S.J.W. performed the experiments and Q.C. helped perform the analysis with constructive discussions.

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