Oxymatrine attenuates hepatic steatosis in non-alcoholic fatty liver disease rats fed with high fructose diet through inhibition of sterol regulatory element binding transcription factor 1 (Srebf1) and activation of peroxisome proliferator activated receptor alpha (Pparα).

The aim of this study was to examine the therapeutic effect of oxymatrine, a monomer isolated from the medicinal plant Sophora flavescens Ait, on the hepatic lipid metabolism in non-alcoholic fatty liver (NAFLD) rats and to explore the potential mechanism. Rats were fed with high fructose diet for 8 weeks to establish the NAFLD model, then were given oxymatrine treatment (40, 80, and 160 mg/kg, respectively) for another 8 weeks. Body weight gain, liver index, serum and liver lipids, and histopathological evaluation were measured. Enzymatic activity and gene expression of the key enzymes involved in the lipogenesis and fatty acid oxidation were assayed. The results showed that oxymatrine treatment reduced body weight gain, liver weight, liver index, dyslipidemia, and liver triglyceride level in a dose dependant manner. Importantly, the histopathological examination of liver confirmed that oxymatrine could decrease the liver lipid accumulation. The treatment also decreased the fatty acid synthase (FAS) enzymatic activity and increased the carnitine palmitoyltransferase 1A (CPT1A) enzymatic activity. Besides, oxymatrine treatment decreased the mRNA expression of sterol regulatory element binding transcription factor 1(Srebf1), fatty acid synthase (Fasn), and acetyl CoA carboxylase (Acc), and increased the mRNA expression of peroxisome proliferator activated receptor alpha (Pparα), carnitine palmitoyltransferase 1A (Cpt1a), and acyl CoA oxidase (Acox1) in high fructose diet induced NAFLD rats. These results suggested that the therapeutic effect of oxymatrine on the hepatic steatosis in high fructose diet induced fatty liver rats is partly due to down-regulating Srebf1 and up-regulating Pparα mediated metabolic pathways simultaneously.

[Effects of inulae and ochrae decoction on the change of rabbits EGG and 5-HT resulted from chemotherapeutic drugs].

AIM: To explore the antagonism mechanism of inulae and ochrae decoction on toxicity damage of gastrointestinal tissue induced by DDP (cisplatin). METHODS: Twenty-four healthy hybrid rabbits were divided into three groups in random: the control group, DDP group, inulae and ochrae decoction + DDP group. The change of rabbits EGG, the concentration of 5-HT,5-HIAA of serum and the content of sinus ventriculi mucosa and the upper part of duodenum tissue were examined. Ultrastructure changes were observed by transmission electron microscope (TEM). RESULTS: The EGG amplitude of DDP group was increased and the frequency was fast (P < 0.05) after i.v. DDP, meanwhile the concentration of 5-HT, 5-HIAA was increased (P < 0.05), and the content of sinus ventriculi mucosa and the upper part of duodenum tissue were higher than that of Inulae and Ochrae Decoction + DDP group (P < 0.05), and the change was seriously under the TEM observing; while inulae and ochrae decoction could prevent the change of EGG caused by DDP, showing the amplitude decreased, and the frequency was slow, and the concentration of 5-HT, 5-HIAA of serum and the content of tissue became lower than that of DDP group. CONCLUSION: Inulae and ochrae decoction could antagonize the change of EGG caused by DDP, which maybe have relations with the over-releasing of gastrointestinal 5-HT.

[iNOS and AChE expression on guinea pigs cochlea spiral ganglion induced by streptomycin and attenuation by Salvia miltiorrhiza injection].

AIM: To study the expression of iNOS and AChE on ginea pigs cochlea spiral ganglion induced by streptomycin (SM) and attenuation by salvia miltiorrhiza injection (Chinese Traditional medicine-dansen DS). METHODS: 32 guinea pigs were divided into 4 groups randomly (n=8): control group, SM group, DS + SM group, DS group. SABC immunohistochemical staining and image quantitative analysis technique were used to observe the expression of iNOS and AChE, as well as grey value analysis, and ABR measurements were used to observe ototoxicity. RESULTS: After 10 days with drugs, the ABR threshold value of SM increased more significantly than that of the control (P < 0.01), while the ABR threshold value of DS+ SM co-treatment increased than the control group, but lower than that of SM group (P < 0.01). The results of immunohistochemical staining implied the expression of iNOS and AChE in SG of SM group were higher than that of control group, and had positive correlate. CONCLUSION: The ABR threshold value increases and the expression of iNOS and AChE strengthen on SM ototoxicity, and has some correlation. DS can attenuate the ototoxicity induced by SM, and has protective function.

[Effect of injection salvia miltiorrhiza on the expression of inducible nitric oxide synthase in the cochlea of guinea pig damaged by streptomycin].

AIM: To investigate the expression of Inducible Nitric Oxide Synthase (iNOS) in the cochlea of guinea pig after streptomycin (SM) and the antagonism of Salvia Miltiorrhiza injection on SM ototoxicity. METHODS: Light microscope, transmission electron microscope (TEM), immunohistochemical staining and image quantitative analysis technique, combined with auditory brainstem response (ABR) measurement were used. RESULTS: After 10 days by drugs, the threshold of ABR of SM increased significantly, and the threshold of ABR of DS+ SM reduced more than that of SM (P < 0.01), the Corti's organ (CO), inner hair cell (IHC) and outer hair cell (OHC), spiral ganglion(SG), stria vascularis (SV) of SM damaged more greatly than that of DS + SM under light microscope and TEM. The result of immunohistochemical staining implied the expression of iNOS in CO, IHC and OHC, SG, SV of SM higher than that of DS+ SM. CONCLUSION: The threshold of ABR increases and the expression of iNOS strengthens on SM ototoxicity. DS can reduce the increasing and inhibit the over-expression of iNOS, and reduce the damage of SM ototoxicity, which implies the protective role of DS on SM ototoxicity.