Objective To study the inhibitory effect of Pharbitidis Semen on rat hepatoma induced by N-nitrosodiethylamine ( NDEA) . Methods SD rats were divided into normal control group, model control group and Pharbitidis Semen group. In model control group and Pharbitidis Semen group, 0. 01% NDEA was applied for 90 days to induce hepatoma, and rats in Pharbitidis Semen group concomitantly received feed containing 6% Pharbitidis Semen at the dosage of 40 g·kg-1 ·d-1 . Thirty days after the hepatoma inducement and Pharbitidis Semen administration, the rats were sacrificed to observe the pathological changes in liver, number of hepatoma nodules and liver weight. The changes of liver/body weight, serum alanine aminotransferase (ALT), γ-glutamyl transferase (γ-GT), and alkaline phosphatase (ALP) were compared. One-way ANOVA (LSD Test) was employed for statistical analysis. Results In the normal control group, the number of hepatoma nodules was 0. 0±0. 0, the liver weight was (9. 87±1. 30) g, the ratio of liver/body weight was (2. 62±0. 24)% and the level of serum ALT was (64. 10±12. 71) U·L-1,γ-GT was (0. 80± 0. 42) U·L-1, and ALP was (121. 20±37. 57) U·L-1. In the model control group, the number of hepatoma nodules was (27. 4±9. 5), the liver weight was (21. 38±7. 29) g, the ratio of liver/body weight was (5. 82±2. 31)%, the level of serum ALT was (175. 70±48. 75) U·L-1, γ-GT was (41. 80±15. 38) U·L-1, and ALP was (200. 50±35. 78) U·L-1. In the Pharbitidis Semen group, the number of hepatoma nodules was (8. 6± 5. 3), the liver weight was (13. 91±3. 55) g, the ratio of liver/body weight was (3. 86±0. 76)% and the level of serum ALT was (113.10±45.35) U·L-1, γ-GT was (13. 40± 6. 15) U·L-1, and ALP was (155. 80±30. 26) U·L-1. The results showed that all indices of Pharbitidis Semen group were higher than those of the normal control group, and lower than those of the model control group (P<0. 01 or P<0. 05). Conclusion Pharbitidis Semen can reduce NDEA-induced injury to the liver cells, and inhibit the overgrowth of the hepatoma.

Objective To observe the Influence of Daotan decoction on nonalcoholic steatohepatitis (NASH) in Rats, and its relative mechanisms was analyzed. Methods The rat nonalcoholic steatohepatitis model was induced by high fat diet. The rats of therapeutic groups were treated with small, middle and high dose Daotan decoction respectively. Their general condition, liver index, and the fat change and inflammation of liver were observed. The serum ALT、triglyceride(TG), total cholesterol(TCH), low density lipoprotein(HCL-C), high density lipoprotein(LDL-C)were determined respectively. Results The liver index of therapeutic groups were markedly reduced respectively compared with those of model group(P0.05). The liver inflammation in therapeutic groups were improved better those in model group(P

(0.05)). The sensitivity and the agreement rate were best at dose of Dob 10 ?g?kg~(-1)?min~(-1) with (86.5)% and (86.5)% (Kappa(0.71)), respectively. When Isoket combined with Dob 3,5 ?g?kg~(-1)?min~(-1), the sensitivities and the agreement rates were both significantly improved than either one used (both P

Objective To explore the effect of ligustrazine on the learning and memory function of rats with aluminum-induced cognitive impairment and its mechanism.Methods Sixty male Wistar rats were divided into a blank control group,a model group,a low-dose ligustrazine group,a high-dose ligustrazine group,and a piracetam group using a random number table method,with 12 rats in each group.The rats in the blank control group were not subjected to any treatment;the rats in the model group,low-dose ligustrazine group,high-dose ligustrazine group,and piracetam group were first prepared with aluminum toxicity models by daily gavage of 100 mg·kg-1 AlCl3 solution.After successful modeling,the rats in the piracetam group were intragastrically administered with piracetam at a dose of 400 mg·kg-1,while rats in the low-dose and high-dose ligustrazine groups were intragastrically administered with 100 and 200 mg·kg-1 ligustrazine,respectively;the rats in the blank control group and the model group were intragastrically administered with the same volume of physiological saline.All rats in the five groups received intragas tric administration once a day for 30 consecutive days.After 30 days of intervention,the Morris water maze test was used to evaluate the learning and memory function of rats in the five groups.After completing the water maze experiment,rats in the five groups were anesthetized with 200 g·L-1 chloral hydrate,and their brain tissues were quickly removed after decapitation.Immunohistochemical staining was used to observe the expression of calcium voltage-gated channel subunit alpha 1E(CACNA1E),calmodulin(CALM),and brain-derived neurotrophic factor(BDNF)in the hippocampal CA1 region of rats in the five groups;Western blot was used to detect the relative expression levels of CACNA1E,CALM,and BDNF proteins in the hippocampal CA1 region of rats in the five groups;and real-time fluorescence quantitative polymerase chain reaction was used to detect the relative expression levels of CACNA1E,CALM,and BDNF mRNA in the hippocampal CA1 region of rats in the five groups.Results On the 1st day of the Morris water maze test,the latent periods of rats in the model group,piracetam group,low-dose ligustrazine group,and high-dose ligustrazine group were significantly higher than those in the blank control group(P＜0.05);there was no statistically significant difference in the latent periods of rats among the piracetam group,low-dose ligustrazine group,high-dose ligustrazine group,and model group(P＞0.05).On the 3rd day of the Morris water maze test,the latent periods of rats in the model group,piracetam group,low-dose ligustrazine group,and high-dose ligustrazine group were significantly higher than those in the blank control group(P＜0.05);the latent periods of rats in the piracetam group and high-dose ligustrazine group were significantly lower than those in the model group and low-dose ligustrazine group(P＜0.05);there was no statistically significant difference in the latent periods of rats between the low-dose ligustrazine group and the model group(P＞0.05).On the 5th day of the Morris water maze test,the latent periods of rats in the model group,piracetam group,low-dose ligustrazine group,and high-dose ligustrazine group were significantly higher than those in the blank control group(P＜0.05);the latent periods of rats in the piracetam group and high-dose ligustrazine group were significantly lower than those in the model group and low-dose ligustrazine group(P＜0.05);there was no statistically significant difference in the latent periods of rats between the low-dose ligustrazine group and the model group(P＞0.05).On the 3rd and 5th days of the Morris water maze test,there was no statistically significant difference in the latent periods of rats between the piracetam group and the high-dose ligustrazine group(P＞0.05).The times of rats crossing platform in the model group,piracetam group,low-dose ligustrazine group,and high-dose ligustrazine group were significantly lower than those in the blank control group,and the times of rats crossing platform in the piracetam group and high-dose ligustrazine group were significantly higher than those in the model group and low-dose ligustrazine group(P＜0.05);there was no statistically significant difference in the times of rats crossing platform between the low-dose ligustrazine group and the model group(P＞0.05);there was no statistically significant difference in the times of rats crossing platform between the piracetam group and the high-dose ligustrazine group(P＞0.05).Under the microscope,brown CACNA1E,CALM,and BDNF positive cells could be observed in the hippocampal CA1 region.The expressions of CACNA1E,CALM,and BDNF proteins in the hippocampal CA1 region of rats in the model group,piracetam group,low-dose ligustrazine group,and high-dose ligustrazine group were significantly lower than those in the blank control group,and the expressions of CACNA1E,CALM,and BDNF proteins in the hippocampal CAl region of rats in the piracetam group and high-dose ligustrazine group were significantly higher than those in the model group and low-dose ligustrazine group(P＜0.05);there was no statistically significant difference in the expressions of CACNA1E,CALM,and BDNF proteins in the hippocampal CAI region of rats between the low-dose ligustrazine group and the model group(P＞0.05);there was no statistically significant difference in the expressions of CACNA1E,CALM,and BDNF proteins in the hippocampal CA1 region of rats between the piracetam group and the high-dose ligustrazine group(P＞0.05).The relative expression levels of CACNA1E,CALM,and BDNF proteins and mRNAs in the hippocampal CA1 region of rats in the model group,piracetam group,low-dose ligustrazine group,and high-dose ligustrazine group were significantly lower than those in the blank control group(P＜0.05);the relative expression levels of CACNA1E,CALM,and BDNF proteins and mRNAs in the hippocampal CA1 region of rats in the piracetam group and high-dose ligustrazine group were significantly higher than those in the model group and low-dose ligustrazine group(P＜0.05);there was no statistically significant difference in the relative expression levels of CACNA1E,CALM,and BDNF proteins and mRNAs in the hippocampal CA1 region of rats between the low-dose ligustrazine group and the model group(P＞0.05);there was no statistically significant difference in the relative expression levels of CACNA1E,CALM,and BDNF proteins and mRNAs in the hippocampal CA1 region of rats between the piracetam group and the high-dose ligustrazine group(P＞0.05).Conclusion Ligustrazine has significant protective effects on aluminum-induced cognitive impairment in rats and can greatly enhance the learning and memory function of rats.The mechanism may be related to the up-regulation of CANA1E,CALM and BDNF expression in the brain induced by ligustrazine.