Neuroprotective effect of gastrodin in methamphetamine-induced apoptosis through regulating cAMP/PKA/CREB pathway in cortical neuron.

OBJECTIVE: Methamphetamine (MA) abuse induces neurotoxicity and causes neuronal cell apoptosis. Gastrodin is a traditional Chinese herbal medicine used for the treatment of nerve injuries, spinal cord injuries, and some central nervous system diseases as well. The present study investigated the neuroprotective effects of gastrodin against MA-induced neurotoxicity in neuronal cells and its potential protective mechanism. METHODS: The primary cortex neuronal culture was divided into four groups (control group, MA group, MA + gastrodin group, and MA + gastrodin + small interfering RNA group). The neurotoxicity of MA was assessed by detecting apoptotic cells by terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling assay and cell viability by cell counting kit 8 (CCK-8) method, the Tuj1-positive cells and the average axonal length were detected by immunofluorescence, and the expressions of cyclic adenosine monophosphate (cAMP), protein kinase A (PKA), cAMP-response element-binding (CREB), and brain-derived neurotrophic factor (BDNF) proteins were detected by Western blot. RESULTS: The results of CCK-8 assay showed that 0.5 mM MA was an optimal concentration that induced neurotoxicity (p < 0.01). Pretreatment with 25 mg/L gastrodin exerted maximum protective effects on neuronal cells. The expression levels of cAMP, PKA, phosphorylated PKA, CREB, phosphorylated CREB, and BDNF proteins were decreased in the MA group, and pretreatment with gastrodin upregulated the expression levels of these proteins (p < 0.01). The expressions of PKA and CREB proteins showed no significant changes in the control group, MA group, and gastrodin group. Compared the MA + gastrodin + small interfering RNA group with MA + gastrodin group, the Tuj1-positive cells and the average axonal length were decreased significantly, while the number of apoptotic cells was increased (p < 0.05). CONCLUSION: Gastrodin has neuroprotective effects against MA-induced neurotoxicity, which exerts neuroprotective effects via regulation of cAMP/PKA/CREB signaling pathway and upregulates the expression of BDNF.

[Textual research on the unclear source of citations from Hua Tuo correlation works cited by the Compendium of Materia Medica].

The Compendium of Materia Medica is a magnum opus, in which a large number of literatures were cited. By searching with keywords, there were 30 citations related with Hua Tuo in this book. However, some citations were not specific, even lack of the source information. The objective of this article is to find out the contents, first-hand source and editions of the primary literatures by doing textual research.As a result, the sources of quotations about the Hua Tuo's Prescription for Madam Pengcheng and Hua Tuo's Emergency Cases Prescriptions were discovered.Meanwhile, it was confirmed that Zhongzang Jing (, Classic of the Central Viscera) with 3 volumes and books of prescriptions during Song and Ming Dynasties were cited by the Compendium of Materia Medica. This solve the long term problem about Hua Tuo's citations, and might benefit further study about the citations of the Compendium of Materia Medica.

[Study on themisprints of the primary version of the Compendium of Materia Medica].

The Jinling version of the Compendium of Materia Medica was the primary version.It accurately represented the ideas of LI Shizhen, therefore it was valued by the scholars.There were many defects in misprint (knife carving) and proofreading.The main errors were some Chinese character's strokes missing and wrong characters printed.The authors collected some statistics data andmade some statistical analysis. They found that total misprints were 376 and emerge 615 times.Those misprints can divide into two categories: lack of some parts of Chinese characters; lack of some strokes of Chinese characters.Four tables which list the misprints was made.It is helpful for scholars to examine Compendium of Materia Medica or the study of other similar ancient literatures.

Comparison of phytase from genetically engineered Aspergillus and canola in weanling pig diets.

Ninety-six crossbred pigs with an average weight of 9.0 kg were used in a 5-wk trial to compare the efficacy of genetically engineered Aspergillus ficuum phytase, expressed in Aspergillus niger (Natuphos) or in canola seed (Phytaseed), for enhancing the utilization of phytate P in corn-soybean meal-based diets fed to young pigs and to evaluate the safety of Phytaseed phytase. Three levels of the two sources of phytase (250, 500, or 2,500 U/kg of diet) were added to a corn-soybean meal basal diet containing .35% total P, .09% available P, and .50% Ca. There were six pens per treatment (one barrow and one gilt/pen), except that the diet without added phytase was fed to 12 pens of pigs. Pen feed consumption and BW were recorded weekly. During wk 5, pen fecal samples were collected for determination of apparent digestibilities of DM, Ca, and P. At the end of wk 5, all barrows were killed, and the 10th rib on both sides was removed for determination of shear force and energy. Thirty pigs (six from the diet without added phytase and the diets with 500 and 2,500 U/kg phytase from both sources) were randomly selected for gross necropsy and histologic evaluation of liver, kidney, and bone tissues. Both sources of phytase were equally effective in increasing (P < .05) daily gain, gain:feed, apparent digestibilities of DM, P, and Ca, and 10th rib measurements. Fecal P excretion was reduced with phytase addition. Feed intake was increased by phytase levels during wk 4 to 5. No significant abnormalities were seen in any of the 30 pigs necropsied. The fit of a nonlinear function revealed that most measurements were reaching a plateau at 2,500 U/kg phytase. In summary, based on performance, bone measurements, and digestibilities of P, Ca, and DM of young pigs, the efficiency of Phytaseed was similar to that of Natuphos for enhancing the utilization of phytate P in corn-soybean meal-based diets. General necropsy and histologic examination of tissues indicated no toxic effect of phytase.

Comparison of genetically engineered microbial and plant phytase for young broilers.

This study was conducted to compare the efficacy of genetically engineered microbial (Natuphos) and plant (Phytaseed) phytase for enhancing the utilization of phytate P in corn-soybean meal-based diets fed to young broilers and to evaluate the safety of Phytaseed phytase. Three levels of each of the two sources of phytase (250, 500, and 2,500 U/kg of diet) were added to a corn-soybean meal basal diet containing 0.46% total P, 0.21% nonphytate P, and 0.92% Ca. There were eight cages per treatment (eight birds per cage for Weeks 2 to 3 and seven birds for Weeks 4 to 5), except for the basal diet without added phytase that had 16 cages. Cage BW and feed consumption were recorded weekly. During Week 5, cage excreta samples were collected for determination of apparent retention coefficients of DM, Ca, and P. At the end of Week 5, all birds were killed, and the left and right toes were removed for determination of toe ash weight and percentage. Forty birds (one per cage from the diet without added phytase and diets with 500 or 2,500 U phytase/kg from both sources) were randomly selected for gross necropsy and histologic evaluation of liver, kidney, and bone tissues. Addition of both sources of phytase resulted in similar increases (P < 0.05) of BW gain; feed intake; gain:feed; apparent retention of DM, P and Ca; and toe measurements. Phosphorus excretion decreased as phytase addition increased. No significant abnormalities were seen in any of the 40 broilers necropsied. Further, the fit of a nonlinear function revealed that most measurements reached a plateau at 2,500 U/kg. Based on performance, bone characteristics, and retention of P, Ca, and DM of young broilers, the efficacy of Phytaseed phytase was similar to that of Natuphos phytase for enhancing the utilization of phytate P in corn-soybean meal-based diets. General necropsy and histologic examination of liver, kidney, and tibial tissues revealed no adverse effects of phytase source or level.

Experimental and clinical studies on the reduction of erythrocyte sorbitol-glucose ratios by ascorbic acid in diabetes mellitus.

In order to confirm the effect of ascorbic acid (AA) on human erythrocyte sorbitol accumulation and explore its mechanism of action, the effects of ascorbic acid in vitro on the sorbitol (S) and glucose (EG) content of human erythrocytes and in particular on the S/EG ratio as a marker of aldose reductase (AR) activity were carefully observed. The results showed that both the accumulation of erythrocyte sorbitol and the S/EG ratio were strongly reduced by the addition of AA. The sorbitol content in the erythrocyte and the S/EG ratio were reduced by a maximum of 87.3% and 83.4% and 93.8% and 63.9% when the medium's AA concentration was at its peak with 5.6 mmol/l and 28 mmol/l glucose in the medium, respectively. The contents of erythrocyte glucose measured coincidentally revealed a positive correlation with the ascorbic acid concentration in the medium during incubation in 5.6 mmol/l glucose while at a higher glucose level (28 mmol/l) in the medium the correlation became negative. These results suggested that the polyol pathway could be inhibited effectively by AA through its direct action on AR. The results of a double-blind cross-over trial using AA tablets or inositol tablets in eight diabetic patients showed that the supplementation of 1000 mg AA/day for 2 weeks resulted in reductions of 12.2% and 21.8% in erythrocyte sorbitol and red cell sorbitol/plasma glucose (S/PG) ratio, respectively (P < 0.05), whereas the fasting plasma glucose levels measured coincidentally revealed no changes (P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

[Reduction of erythrocyte sorbitol by ascorbic acid in patients with diabetes mellitus].

The content of erythrocyte sorbitol could be reduced by ascorbic acid (AA). To confirm the effect of AA on human erythrocyte sorbitol accumulation and explore its mechanism of the action, we studied in vitro the effects of ascorbic acid on the contents of both sorbitol and glucose in human erythrocytes. The effect of AA on the ratio of sorbitol to glucose in erythrocyte (S/EG) which was referred to as a marker of aldose reductase (AR) activity was observed. Both the accumulation of erythrocyte sorbitol and S/EG were reduced by the addition of ascorbic acid (AA) during in vitro incubations. The sorbitol content in the erythrocyte and S/EG were reduced by a maximum of 87.3%, 83.4% and 93.8%, 63.9% when the medium's AA concentration was at its peak in the 5.6 mmol/L and 28 mmol/L glucose concentration of medium respectively. These suggested that the activity of polyol pathway could be inhibited effectively by AA which might directly act on the activity of AR. The results of a double-blind cross-over trial using AA tablets or inert inositol tablets in 8 diabetic patients showed that the supplementation of 1,000 mg AA/day continued for 2 weeks resulted in reductions of 12.2% and 21.8% in both erythrocyte sorbitol and red cell sorbitol: plasma glucose (S/PG) ratio, respectively (P < 0.05). The fasting plasma glucose levels measured coincidently revealed no changes (P > 0.05). This suggests that the supplementation of moderate AA (1,000 mg/day) might provide a simple, safe and effective means of preventing and ameliorating chronic complications of diabetes.