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Four new 3, 4-seco-labdane diterpenoids, nudiflopenes J-M, were isolated from the leaves of Callicarpa nudiflora along with six known compounds. The structures of these diterpenoids were determined by comprehensive spectroscopic analysis. All the isolated compounds were evaluated for their inhibitory effects on NO production in LPS-stimulated RPMs and RAW264.7 cells. The results suggest that nudiflopenes J-M and other four known compounds showed significant inhibitory effects against NO production comparable to the positive control dexamethasone.
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Objective To investigate the protective effect and the mechanism of amitriptyline on sepsis-induced kidney injury.Methods 48 male Sprague Dawley (SD) rats were randomly divided into six groups:sham group,sham + saline group,sham + amitriptyline group,sepsis group,sepsis + saline group,sepsis + amitriptyline group.Sepsis model was induced by cecal ligation and puncture (CLP).Sham group did not undergo CLP.Amitriptyline were injected subcutaneously to rats with amitriptyline 3 mg/kg before treatment for 10 d,2 times/d,while the control group was injected with the same amount of normal saline.Blood sample was obtained to detect serum level of acid sphingomyelinase (ASMase),ceramide,blood urea nitrogen (BUN),creatinine and interleukin-1β.Malondialdehyde in kidney tissue was determined,and Kidney hematoxylin eosin (HE) staining was performed to observe pathologic change.Another 48 rats were randomly divided into four groups:sham group,sepsis group,sepsis + saline group,sepsis + amitriptyline group.The intervention to each group were same as above description.Rats of the four groups were observed for seven days to determine the survival rate.Results The survival rate of rats in sham group were 100％,the survival rate of the sepsis group and the sepsis + physiological saline group was less than 20％,while the survival rate of the sepsis + amitriptyline group was ＞ 50％.The serum concentration of IL-1β,ceramide,BUN,SCr,the activity of ASMase and the level of malondialdehyde (MDA) in kidney tissue were respectively increased in sepsis group,sepsis + saline group and sepsis + amitriptyline group at the 4 time points were significantly higher than the sham groups (P ＜0.01),these indexes in sepsis plus amitriptyline group were significantly decreased compared to sepsis group (P ＜ 0.01).There was no pathologic change in sham group,sham + saline group and sham + amitriptyline group.In sepsis group and sepsis + saline group,general degeneration and necrosis of renal proximal tubular epithelial cells,marked dilatation of renal tubular capsular space,extensive infiltration of inflammatory cells and hemorrhage in renal interstitium were observed.These pathologic changes were obviously reduced in sepsis + amitriptyline group compared with sepsis group.Conclusions Amitriptyline can alleviate sepsis-induced kidney injury,through inhibiting the activity of ASMase and then restraining inflammatory response and oxidative stress in renal tissues.
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The compounds were isolated and purified by HP20 macroporous adsorption resin, ODS, silica gel, and Sephadex LH-20 column chromatography, as well as semi-preparative HPLC chromatography from the 80% ethanol extract of the root of Angelica decursiva, and their structures were identified based on their physiochemical properties and spectroscopic data. Twelve compounds were structures were identified as (9R,10R)-9-acetoxy-8,8-dimethyl-9,10-dihydro-2H,8H-benzo[1,2-b：3,4-b']dipyran-2-one-10-yl ester (1), bakuchicin (2), (3', S,4'S)-disenecioyloxy-3',4'-dihydroseselin (3), (3'R,4'R)-3'-angeloyloxy-4'-senecioyloxy-3',4'-dihydroseselincalipteryxin (4), (+)-8,9-dihydro-8-(2-hydroxypropan-2-yl)-2-oxo-2H-furo[2,3h]chromen-9-yl-3-methylbut-2-enoate (5), libanoridin (6), selinidin (7), suberosin (8), crocatone (9), peujaponisinol B (10), peujaponisinol A (11), and ostenol (12), respectively. Compounds 1-5 were isolated from the plants of Angelica genus for the first time. Compounds 7-12 were isolated from A. decursiva for the first time.
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Objective To investigate the clinical efficacy of acupuncture at point Shanzhong(CV17) plus cupping on Back-Shu points in treating migraine. Methods Seventy migraine patients were randomly allocated to treatment and control groups, 35 cases each. The control group received conventional acupuncture and the treatment group, acupuncture at point Shanzhong(CV17) plus cupping on Back-Shu points in addition. The VAS score was counted in the two groups before and after treatment. The clinical therapeutic effects were compared between the two groups. Results The cure and marked efficacy rate and the total efficacy rate were 88.6%and 100.0%, respectively, in the treatment group and 62.9%and 94.3%, respectively, in the control group. There was a statistically significant difference in the cure and marked efficacy rate between the two groups (P＜0.05). There was a statistically significant pre-/post-treatment difference in the VAS score in the two groups (P＜0.05). There was a statistically significant post-treatment difference in the VAS score between the treatment and control groups (P>0.01). The clinical symptom improvement rate was (78.3±10.6)%in the treatment group and (49.8±11.2)%in the control group;there was a statistically significant difference between the two groups (P＜0.01). Conclusion Acupuncture at point Shanzhong plus cupping on Back-Shu(CV17) points is an effective way to treat migraine.
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<p><b>OBJECTIVE</b>To investigate the effect of everolimus(RAD001)combined with all-trans retinoid acid(ATRA) on drug resistance of ATRA-resistance acute promyelocytic leukemia(APL) cell line NB4-R1 and its molecular mechanism.</p><p><b>METHODS</b>APL NB4-R1 cells were treated with different concentrations of RAD001(1 nmol/L, 10 nmol/L and 100 nmol/L) with ATRA(1μmol/L) for 24, 48 and 72 h, respectively. The differentiation of NB4-R1 cells was analyzed by flow cytometry with CD11b staining and nitro blue tetrozolium(NBT) reduction test. Cell cycle was detected by cell cycle staining kit and apoptosis was detected by flow cytometry with Annexin V/PI staining. Protein expressions of LC-3II, PML-RARα, P-P70S6K and P-4E-BP1 were determined by Western blotting.</p><p><b>RESULTS</b>RAD001 combined with ATRA significantly induced NB4-R1 cells differentiation, but RAD001 or ATRA alone did not enhance NB4-R1 differentiation. The co-treatment induced accumulation of cells in G1 phase and decreased the proportion of cells in S phase. The combined treatment had no effect on cell apoptosis. The differentiation rate of NB4-R1 cells in 100 nmol/L RAD001, 1μmol/L ATRA, RAD001 combined with ATRA and control groups was(2.29±0.57)%,(17.06±2.65)%,(54.47±4.91)% and(2.54±0.53)%, respectively; the proportion of cells in G1 phase was(35.20±11.97)%,(33.54±6.25)%,(53.70±8.73)% and(27.40±6.01)%, respectively; cells apoptosis rate was(2.30±0.14)%,(2.25±0.21)%,(2.40±0.28)% and(1.95±0.07)%, respectively. The combination of RAD001 with ATRA significantly inhibited mTOR signaling downstream proteins P-P70S6K, P-4E-BP1 and enhanced autophagy-related protein LC3-II and Beclin 1. The co-treatment also induced degradation of fusion protein PML-RARα.</p><p><b>CONCLUSION</b>RAD001 combined with ATRA can induce cell differentiation, inhibit cell cycle, resulting the reverse of drug resistance in NB4-R1 cells, which is associated with increase of autophagy level and degradation of PML-RARα.</p>