[Atractylenolide â improves acetaminophen-induced acute liver injury in mice by inhibiting MAPK/NF-κB signaling pathway].

This study explored the protective effect of atractylenolide Ⅰ(AO-Ⅰ) against acetaminophen(APAP)-induced acute liver injury(ALI) in mice and its underlying mechanism. C57 BL/6 J mice were randomly divided into a control group, an APAP group(500 mg·kg~(-1)), a low-dose combination group(500 mg·kg~(-1) APAP + 60 mg·kg~(-1) AO-Ⅰ), and a high-dose combination group(500 mg·kg~(-1) APAP + 120 mg·kg~(-1) AO-Ⅰ). ALI was induced by intraperitoneal injection of APAP(500 mg·kg~(-1)). AO-Ⅰ by intragastric administration was performed 2 hours before APAP treatment, and the control group received the same dose of solvent by intragastric administration or intraperitoneal injection. The protective effect of AO-Ⅰ against APAP-induced ALI was evaluated by detecting alanine aminotransferase(ALT) and aspartate aminotransferase(AST) levels in the plasma and H&E staining in liver tissues of mice. The malondialdehyde(MDA) and glutathione(GSH) content and catalase(CAT) activity in mouse liver tissues were detected to evaluate the effect of AO-Ⅰ on APAP-induced oxidative stress in the liver. The proteins in the liver p38 mitogen-activated protein kinase(p38 MAPK), c-jun N-terminal kinase(JNK), and nuclear factor kappa-B p65(NF-κB p65) signaling pathways were measured by Western blot, and the liver inflammatory cytokines interleukin-1ß(IL-1ß) and interleukin-6(IL-6) were detected by real-time PCR. Compared with the APAP group, the combination groups showed reduced APAP-induced ALT level and liver MDA content, potentiated liver CAT activity, and elevated GSH content. Mechanistically, AO-Ⅰ treatment significantly inhibited APAP-up-regulated MAPK phosphorylation and NF-κB p65, and significantly reduced the transcriptional activities of IL-1ß and IL-6, downstream targets of NF-κB p65. AO-Ⅰ can improve APAP-induced ALI and the underlying mechanism is related to the inhibition of the MAPK/NF-κB p65 signaling pathway in APAP-challenged mice.

[Mechanisms of tanshinone â ¡_A in reducing 4-HNE-induced hepatocyte damage by activating PPARα].

Tanshinone Ⅱ_A( Tan Ⅱ_A),the liposoluble constituents of Salvia miltiorrhiza,can not only ameliorate the lipidic metabolism and decrease the concentration of lipid peroxidation,but also resist oxidation damage,scavenge free radicals and control inflammation,with a protective effect on prognosis after liver function impairment. Therefore,the studies on the exact mechanism of Tan Ⅱ_A in protecting the liver can provide important theoretical and experimental basis for the prevention and treatment effect of Tan Ⅱ_A for liver injury. In the present study,the protective effects and mechanism of Tan Ⅱ_A on 4-hydroxynonenal( 4-HNE)-induced liver injury were investigated in vitro. Normal liver tissues NCTC 1469 cells were used to induce hepatocytes oxidative damages by 4-HNE treatment. The protective effect of Tan Ⅱ_A on hepatocytes oxidative damages was detected by release amount of lactate dehydrogenase( LDH) analysis and hoechst staining. The protein expression changes of peroxisome proliferator-activated receptor α( PPARα) and peroxisome proliferator response element( PPRE) were analyzed by Western blot analysis in NCTC 1469 cells before and after Tan Ⅱ_A treatment. The gene expression changes of fatty aldehyde dehydrogenase( FALDH) were analyzed by Real-time polymerase chain reaction( PCR) analysis. The results showed that 4-HNE increased the release amount of LDH,lowered the cell viability of NCTC 1469 cells,and Tan Ⅱ_A reversed 4-HNE-induced hepatocyte damage. Western blot analysis and RT-PCR analysis results showed that 4-HNE decreased the expression of PPARα and FALDH and increased the expression of 4-HNE. However,the expression of PPARα and FALDH were increased significantly and the expression of 4-HNE was decreased obviously after Tan Ⅱ_A treatment. This study confirmed that the curative effect of Tan Ⅱ_A was obvious on hepatocytes damage,and the mechanism may be associated with activating PPARα and FALDH expression as well as scavenging 4-HNE.

[Pharmacognostical study of Cyperus rotundus growing in Wen-River area].

OBJECTIVE: To study the macroscopic, microscopic identification and chemical components of Cyperus rotundus growing in Wen-River area. METHODS: The features of different parts of Cyperus rotundus were described by material morphology and microscopic identification, the chemical components of aerial part and rhizome of Cyperus rotundus were studied by chemical experiment and GC-MS analysis. RESULTS: Summarized the transverse section structure of rhizome, stem and leaf of Cyperus rotundus, the chemical components of aerial part and the components and relative content of volatile oil in rhizome were determined. CONCLUSION: This study provides reference for the drug identification and the daodi medicinal material exploitation of Cyperus rotundus.

[Longchang granule upregulates the expression of bax in the prostatic hyperplastic tissues of rats].

OBJECTIVE: To investigate the mechanism of Longchang Granule in the treatment of benign prostatic hyperplasia. METHODS: Rat models of prostate hyperplasia were made by castration and testosterone propionate injection. After treated respectively with Longchang Granule and Longbishu by gastrogavage for 30 days, all the model rats were killed and their prostate glands harvested for the measurement of the wet weight and detection of the expression of bax in the prostatic hyperplastic tissues by RV 2-step method. RESULTS: The wet weight of the prostate was (0.61 +/- 0.03) g in the blank control group, (0.95 +/- 0.04) g in the model group, (0.73 +/- 0.02) g in the Longbishu group, (0.80 +/- 0.05) g in the low-dose Longchang group, (0.78 +/- 0.07) g in the medium-dose Longchang group and (0.68 +/- 0.03) g in the high-dose Longchang group, with significant differences between the model and the intervention groups (P < 0.05). The prostate indexes in the above groups were 0.143 +/- 0.006, 0.226 +/- 0.008, 0.172 +/- 0.004, 0.199 +/- 0.012, 0.181 +/- 0.010 and 0.168 +/- 0.003, respectively, and the expressions of bax by mean optical density were 0.226 +/- 0.010, 0.184 +/- 0.005, 0.206 +/- 0.015, 0.199 +/- 0.001, 0.202 +/- 0.003 and 0.211 +/- 0.003, respectively, both with significant differences between the model and the intervention groups (P < 0.05). CONCLUSION: Longchang Granule can effectively reduce the wet weight of the prostate and alleviate its pathological changes in BPH rats, the mechanism of which may be associated with its effect of upregulating the expression of bax and accelerating cell apoptosis in the prostate tissues.