Berberine attenuates cognitive dysfunction and hippocampal apoptosis in rats with prediabetes.

The cognitive dysfunction caused by prediabetes causes great difficulties in human life, and the terrible thing is that the means to prevent the occurrence of this disease are very limited at present, Berberine has shown the potential to treat diabetes and cognitive dysfunction, but it still needs to be further explored to clarify the mechanism of its therapeutic effect. Therefore, the aim of this study was to investigate the effects and mechanisms of Berberine on prediabetes-induced cognitive dysfunction. Prediabetes rat model was induced by a high-fat diet and a normal diet was used as a control. They were fed for 20 weeks. At week 13, the model rats were given 100 mg/kg Berberine by gavage for 7 weeks. The cognitive function of rats was observed. At the same time, OGTT, fasting blood glucose, blood lipids, insulin and other metabolic parameters, oxidative stress, and apoptosis levels were measured. The results showed that the model rats showed obvious glucose intolerance, elevated blood lipids, and insulin resistance, and the levels of oxidative stress and apoptosis were significantly increased. However, after the administration of Berberine, the blood glucose and lipid metabolism of prediabetic rats were significantly improved, and the oxidative stress level and apoptosis level of hippocampal tissue were significantly reduced. In conclusion, Berberine can alleviate the further development of diabetes in prediabetic rats, reduce oxidative stress and apoptosis in hippocampal tissue, and improve cognitive impairment in prediabetic rats.

[Nicotine regulates large conductance ca2+ activated K+ channels in rat coronary arterial smooth muscle cells].

OBJECTIVE: The present study was to explore signaling mechanisms underlying nicotine-induced inhibition of large-conductance calcium-activated potassium channels (BK(Ca)). METHODS: 8 week male Wistar rats were divided randomly into saline group and nicotine group and received respectively injection with saline or nicotine (Sigma, Shanghai, China) at 2 mg/(kg x d) for 21 days. Coronary vascular smooth muscle cells were dissociated enzymatically. Dissociated smooth muscle cells were interfered with CPT-cAMP (100 micromol/L) or forskolin (10 micromol/L). The signal channel open dwell-time (To), close dwell-time (Tc) and open probability (Po) were recorded. RESULTS: CPT-cAMP or forskolin significantly prolonged To, shorten Tc and increased Po in saline group (P < 0.01). But in nicotine group To, Tc and Po did not been changed. CONCLUSION: This phenomenon may serve as a physiological mechanism that nicotine inhibits BK(Ca) channel activity to increase via cAMP/PKA-dependent pathway.

[Correlation of plasma endothelin and multiple organ dysfunction syndrome caused by acute paraquat poisoning].

OBJECTIVE: To investigate the relationship between endothelin (ET) and multiple organ dysfunction syndrome (MODS) caused by acute paraquat poisoning (APP). METHODS: The levels of plasma ET were measured by radioimmunoassay in 24 patients with MODS caused by APP and 19 healthy persons as controls. The levels of plasma ET patients in MODS caused by APP were correlatively analysed with acute physiology and chronic health evaluation II (APACHE II) score, partial pressure of oxygen in artery (PaO2), troponin I (cTnI) level, blood enzymology and biochemistry indexes. RESULTS: The levels of plasma ET in patients with MODS caused by APP were much higher than controls (P<0.01), the level of plasma ET in death group was much higher than that of survivor group (P<0.01). Plasma ET was positively correlated with APACHE II score, cTnI, MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH), alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN) and serum creatinine (SCr, P<0.05 or P<0.01), where there was a negative correlation with PaO2 (P<0.01). CONCLUSION: Endothelin may be involved in the pathogenesis of MODS caused by APP, plasma ET may be one of a clinical index for evaluating the degree of multiple organ function damage, for guiding treatment, and judging the prognosis of MODS caused by APP.