Electroacupuncture Ameliorates Depressive-Like Behaviors in Poststroke Rats via Activating the tPA/BDNF/TrkB Pathway.

BACKGROUND: Electroacupuncture (EA) is a form of physical therapy that has been widely used in clinical practice in China. Post-stroke depression (PSD) is the most common neuropsychiatric complication after stroke. EA has been shown to have beneficial effects on PSD patients. However, the potential mechanism underlying the protective effects of EA on PSD remains unclear. Here, we investigated whether tissue plasminogen activator (tPA)/brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrkB) signaling pathway participates in the therapeutic effects of EA in a rat PSD model. METHODS: Experimental PSD was induced by combining middle cerebral artery occlusion (MCAO) with chronic unpredictable mild stimulation (CUMS) in adult male rats. Bodyweight gain, neurological score, sucrose preference, and open field test were determined at 0, 7, 14, and 35 days after completing MCAO. The protein expressions of tPA, precursor BDNF (proBDNF), mature BDNF (mBDNF), and TrkB were measured by immunofluorescence and Western blot analysis. The tPA inhibitor plasminogen inhibitor-1 (PAI-1) was used to explore whether tPA plays a crucial role in the protective effects of EA on PSD. RESULTS: Compared with the sham rats, the PSD rats showed decreased bodyweight, deteriorated neurological score, and significant depressive-like behaviors. EA remarkably reversed bodyweight loss, neurological deficit, and depressive-like behaviors in PSD rats. Immunofluorescence staining and Western blot analysis showed that PSD-induced decreased expression of tPA, mBDNF, and TrkB were prevented by EA. Furthermore, we found that the effects of EA against PSD-induced depressive-like behaviors were abolished by PAI-1, the specific inhibitor of tPA. CONCLUSION: Our results suggest that the improvement in depressive-like behaviors induced by EA is likely achieved via activation of the tPA/BDNF/TrkB pathway.

Huang-lian-jie-du-decoction modulates glucagon-like peptide-1 secretion in diabetic rats.

AIM OF THE STUDY: Huang-lian-jie-du-decoction (HLJDD), a well-known Chinese herbal formula, has been used for diabetic treatment. The purpose of the study was to investigate whether HLJDD affected glucagon-like peptide (GLP)-1 (7-36) amide level in diabetic rats. MATERIALS AND METHODS: Streptozotocin (STZ)-induced diabetic rats were treated with HLJDD at low dose (2 g/kg/day) or high dose (4 g/kg/day). After 5-week treatment, GLP-1 (7-36) amide level and insulin level in portal vein and tissues stimulated by oral glucose load were measured by ELISA kits. The proglucagon gene expression in intestinal tracts and the proliferation of intestinal L cell and pancreatic beta cell were measured using RT-PCR and immunohistochemistry techniques, respectively. RESULTS: It was found that 5-week HLJDD treatment attenuated alteration of glucose level and insulin level in plasma and tissues of diabetic rats induced by STZ, accompanied by improvement of diabetic syndrome. 5-week HLJDD treatment increased GLP-1 (7-36) amide level in portal vein plasma and distal ileum. Further studies showed that 5-week HLJDD treatment increased the mRNA level of proglucagon gene in distal ileum, promoted pancreatic beta cell and intestinal L cell proliferation in a dose-dependent manner. CONCLUSION: All the results indicated that HLJDD exerted its anti-diabetic effects partly via modulating GLP-1 (7-36) amide level.

Berberine promotes glucagon-like peptide-1 (7-36) amide secretion in streptozotocin-induced diabetic rats.

Berberine (BBR), a hypoglycemic agent, has shown beneficial metabolic effects for anti-diabetes, but its precise mechanism was unclear. Glucagon-like peptide-1 (GLP-1) is considered to be an important incretin that can decrease hyperglycemia in the gastrointestinal tract after meals. The aim of this study was to investigate whether BBR exerts its anti-diabetic effects via modulating GCG secretion. Diabetes-like rats induced by streptozotocin received BBR (120 mg/kg per day, i.g) for 5 weeks. Two hours following the last dose, the rats were anaesthetized and received 2.5 g/kg glucose by gavage. At 15-minute and 30-minute after glucose load, blood samples, pancreas, and intestines were obtained to measure insulin and GCG using ELISA kit. The number of L cells in the ileum and beta-cells in the pancreas were identified using immunohistology. The expression of proglucagon mRNA in the ileum was measured by RT-PCR. The results indicated that BBR treatment significantly increased GCG levels in plasma and intestine (P<0.05) accompanied with the increase of proglucagon mRNA expression and the number of L-cell compared with the controls (P<0.05). Furthermore, BBR increased insulin levels in plasma and pancreas as well as beta-cell number in pancreas. The data support the hypothesis that the anti-diabetic effects of BBR may partly result from enhancing GCG secretion.