Residue and dissipation kinetics of toosendanin in cabbage, tobacco and soil using IC-ELISA detection.

Toosendanin (TSN), as an important Chinese traditional insecticide, has been registered and commercialized in China. In this report, the residual analytical methods, residue dynamics and final residues of TSN in tobacco, cabbage and soil under field condition were studied by IC-ELISA and HPLC. The sensitivity, precision and repeatability of IC-ELISA method were more suitable in comparison with HPLC for the demand of TSN residue analysis. Using IC-ELISA, the half-lives (t1/2) of TSN were found to be 1.30 days in cabbage, 1.70 days in tabacco and 0.71 days in soil, respectively. At the recommended dose, the final residues of TSN detection by IC-ELISA was 0.009 mg·kg-1 in cabbage and 0.043 mg·kg-1 in tobacco, as well as was not detected in soil. Therefore, TSN is easily degradable, and IC-ELISA could be a convenient and supplemental analytical tool for monitoring TSN residue in crops and environment.

Inulin supplementation ameliorates hyperuricemia and modulates gut microbiota in Uox-knockout mice.

PURPOSE: Inulin is a type of fermentable dietary fiber, which is non-digestible, and can improve metabolic function by modulating intestinal microbiota. This study aimed to evaluate the role of inulin in hyperuricemia and microbial composition of the gut microbiota in a mouse model of hyperuricemia established through knockout of Uox (urate oxidase) gene. METHODS: KO (Uox-knockout) and WT (wild-type) mice were given inulin or saline by gavage for 7 weeks. The effect of inulin to combat hyperuricemia was determined by assessing the changes in serum UA (uric acid) levels, inflammatory parameters, epithelial barrier integrity, fecal microbiota alterations, and SCFA (short-chain fatty acid) concentrations in KO mice. RESULTS: Inulin supplementation can effectively alleviate hyperuricemia, increase the expressions of ABCG2 in intestine, and downregulate expression and activity of hepatic XOD (xanthine oxidase) in KO mice. It was revealed that the levels of inflammatory cytokines and the LPS (lipopolysaccharide) were remarkably higher in the KO group than those in the WT group, indicating systemic inflammation of hyperuricemic mice, but inulin treatment ameliorated inflammation in KO mice. Besides, inulin treatment repaired the intestinal epithelial barrier as evidenced by increased levels of intestinal TJ (tight junction) proteins [ZO-1 (zonula occludens-1) and occluding] in KO mice. Moreover, serum levels of uremic toxins, including IS (indoxyl sulfate) and PCS (p-cresol sulfate), were reduced in inulin-treated KO mice. Further investigation unveiled that inulin supplementation enhanced microbial diversity and raised the relative abundance of beneficial bacteria, involving SCFAs-producing bacteria (e.g., Akkermansia and Ruminococcus). Additionally, inulin treatment increased the production of gut microbiota-derived SCFAs (acetate, propionate and butyrate concentrations) in KO mice, which was positively correlated with the effectiveness of hyperuricemia relief. CONCLUSIONS: Our findings showed that inulin may be a promising therapeutic candidate for the treatment of hyperuricemia. Moreover, alleviation of hyperuricemia by inulin supplementation was, at least, partially conciliated by modulation of gut microbiota and its metabolites.

Panax notoginseng saponins inhibits atherosclerotic plaque angiogenesis by down-regulating vascular endothelial growth factor and nicotinamide adenine dinucleotide phosphate oxidase subunit 4 expression.

OBJECTIVE: To investigate the mechanism of Panax notoginseng saponins (PNS), an effective component extracted from Panax notoginseng, on atherosclerotic plaque angiogenesis in atherosclerosis-prone apolipoprotein E-knockout (ApoE-KO) mice fed with high-fat, high-cholesterol diet. METHODS: Twenty ApoE-KO mice were divided into two groups, the model group and the PNS group. Ten normal C57BL/6J mice were used as a control group. PNS (60 mg/kg) was orally administered daily for 12 weeks in the PNS group. The ratio of plaque area to vessel area was examined by histological staining. The tissue sample of aortic root was used to detect the CD34 and vascular endothelial growth factor (VEGF) expression areas by immunohistochemistry. The expression of VEGF and nicotinamide adenine dinucleotide phosphate oxidase subunit 4 (NOX4) were measured by reverse transcription polymerase chain reaction and Western blotting respectively. RESULTS: After treatment with PNS, the plaque areas were decreased (P<0.05). CD34 expressing areas and VEGF expression areas in plaques were significantly decreased (P<0.05). Meanwhile, VEGF and NOX4 mRNA expression were decreased after treatment with PNS. VEGF and NOX4 protein expression were also decreased by about 72% and 63%, respectively (P<0.01). CONCLUSION: PNS, which decreases VEGF and NOX4 expression, could alleviate plaque angiogenesis and attenuate atherosclerosis.

Qindan capsule changes adventitial collagen synthesis in spontaneously hypertensive rats.

OBJECTIVE: To investigate the effect of Qindan capsule (QC) on collagen synthesis and the mechanism underlying the process in spontaneously hypertensive rats (SHRs). METHODS: Twentyfour SHRs were divided into three groups: the hypertension model group, the QC treatment group, and the losartan treatment group. Eight Wistar Kyoto (WKY) rats were used as the normal control group. The systolic blood pressure (SBP) of the rats was monitored, and the thoracic aorta adventitia of the rats was segregated. The expressions of transforming growth factor 1 (TGF-ß1), Smad3, and collagens I and were measured by histological staining and reverse transcription polymerase chain reaction. RESULTS: The SBP was significantly higher in the model group than in the normal control group (P<0.01). However, a significant SBP-lowering effect was observed in QC or losartan treatment groups (P<0.05 or P<0.01) after 3 weeks of treatment. QC-treated rats showed a decrease of approximately 40 mm Hg, and the losartan-treated rats showed a decrease of approximately 50 mm Hg at the end of treatment compared with the beginning of treatment. The protein and gene levels of TGF-ß1, Smad3, and collagens I and in the model group were significantly increased compared with those in the normal control group (P<0.01). However, the levels were significantly decreased in the QC or losartan treatment group compared with the model group (P<0.05 or P<0.01). However, there was no significant difference between the QC and losartan treatment groups (P<0.05). CONCLUSIONS: QC could exert its antihypertensive effect through down-regulating TGF-ß1-stimulated collagen expressions. The TGF-ß1/Smad3 signaling pathway may be involved in this process.

Qindan-capsule inhibits proliferation of adventitial fibroblasts and collagen synthesis.

AIMS: Qindan-capsule (QC) is a prescription of traditional Chinese medicine for the treatment of hypertension. We investigated the effect and mechanism of QC-containing serum on proliferation of aortal adventitial fibroblasts (AFs) and composition of extracellular matrix (ECM). We also tested whether the Smad3 signaling pathway is activated in the progress. MATERIALS AND METHODS: AFs were cultured by tissue explant in vitro. The proliferation of AFs induced by transforming growth factor beta1 (TGF-beta1) and affected by QC-containing serum with high or low dose was detected by MTT. The protein and mRNA expressions of Smad3 and Procollagen I were observed by Western blot and Real-time PCR respectively. RESULTS: Western blot and Real-time PCR revealed that after being activated by TGF-beta1 for 24h, the expressions of Smad3, Pho-Smad3 and Procollagen I were all higher than those in the control group. But these functions were inhibited, to some extent in different doses, by QC-containing serum. So that the proliferation of AFs which was evaluated by MTT. CONCLUSIONS: The results suggested QC-containing serum has significantly improved proliferation of AFs and composition of extracellular matrix. TGF-beta1/Smad3 signaling pathway may be involved in the mechanism.

Total panax notoginsenosides prevent atherosclerosis in apolipoprotein E-knockout mice: Role of downregulation of CD40 and MMP-9 expression.

Total panax notoginsenosides (TPNS) are the main active ingredients in San-Chi, the root of Panax notoginseng (Burk) F.H. Chen, which belongs to the Araliaceae family and has been used in traditional Chinese medicine to treat atherosclerosis. We investigated the effect of TPNS on serum lipid levels and cell differentiation antigen 40 (CD40) and matrix metalloproteinase 9 (MMP-9) expression in atherosclerosis in apolipoprotein E-knockout (apoE-KO) mice fed a high-fat, high-cholesterol diet. Twenty-four apoE-KO mice were divided into two groups, the ApoE-KO group and the ApoE-KO + TPNS group. TPNS (60 mg/kg) was orally administered daily for 12 weeks in ApoE-KO + TPNS group. After 12 weeks, blood and aortas were obtained. Serum levels of lipid were analyzed, serum oxidized low density lipoprotein (oxLDL) concentration, ratio of plaque area-to-vessel area and the expression of CD40 and MMP-9 were examined by ELISA, histological staining, immunohistochemistry and real-time PCR, respectively. It was observed in our study that serum levels of lipid and oxLDL, ratio of plaque area to vessel area, and expression of CD40 and MMP-9 were lower in the ApoE-KO + TPNS group than in the ApoE-KO group. These results suggest that TPNS could prevent atherosclerosis by lowering serum lipid levels and regulating vascular CD40 and MMP-9 expression. TPNS may have implications for clinical treatment of atherosclerosis vascular disease.

Inhibitory effect of Ginkgo biloba extract on hyperhomocysteinemia-induced intimal thickening in rabbit abdominal aorta after balloon injury.

Ginkgo biloba extract (GBE) has been widely used to treat cardiovascular and cerebrovascular disorders. Hyperhomocysteinemia (Hhcy) is associated with the risk of atherosclerosis and restenosis after angioplasty. The objective of this study was to investigate whether GBE could attenuate the Hhcy-induced intimal thickening after balloon injury in rabbit abdominal aorta. It was observed in this study that GBE could decrease the neointima area (NA) and the ratio of the neointima area to the media area (NA/MA), down-regulate the mRNA expression of matrix metalloproteinase-9 (MMP-9) and up-regulate the protein expression of p21 (WAF1/CIP1) (p21). It suggests that GBE can reverse the Hhcy-induced neointima formation in rabbits following balloon injury, and the suppressive effect of GBE on the migration and proliferation of vascular smooth muscle cells (VSMCs) may contribute to its actions.