maximised curcuminoids 5g to 8g (good for pain)
green tea 3g
I have been taking the above for 3 weeks since my latest steroids session. So far the pain in my left leg has improved and I have had very few night spasms. My walking remains poor and limited to a max of 400meters possibly less.
I am also taking a fibrinolytic called lumbrokinase and a combination of serrapeptase and nattokinase again for their fibrinolytic properties.
1: Mol Carcinog. 2002 Mar;33(3):137-45. Links
The chemopreventive compound curcumin is an efficient inhibitor of Epstein-Barr virus BZLF1 transcription in Raji DR-LUC cells.Hergenhahn M, Soto U, Weninger A, Polack A, Hsu CH, Cheng AL, Rösl F.
Division of Genetic Alterations in Carcinogenesis, Deutsches Krebsforschungszentrum, Heidelberg, Germany.
To characterize the effects of inhibitors of Epstein-Barr virus (EBV) reactivation, we established Raji DR-LUC cells as a new test system. These cells contain the firefly luciferase (LUC) gene under the control of an immediate-early gene promoter (duplicated right region [DR]) of EBV on a self-replicating episome. Luciferase induction thus serves as an intrinsic marker indicative for EBV reactivation from latency. The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) induced the viral key activator BamH fragment Z left frame 1 (BZLF1) protein ("ZEBRA") in this system, as demonstrated by induction of the BZLF1 protein-responsive DR promoter upstream of the luciferase gene. Conversely, both BZLF1 protein and luciferase induction were inhibited effectively by the chemopreventive agent curcumin. Semiquantitative reverse transcriptase (RT)-polymerase chain reaction (PCR) further demonstrated that the EBV inducers TPA, sodium butyrate, and transforming growth factor-beta (TGF-beta) increased levels of the mRNA of BZLF1 mRNA at 12, 24, and 48 h after treatment in these cells. TPA treatment also induced luciferase mRNA with similar kinetics. Curcumin was found to be highly effective in decreasing TPA-, butyrate-, and TGF-beta-induced levels of BZLF1 mRNA, and of TPA-induced luciferase mRNA, indicating that three major pathways of EBV are inhibited by curcumin. Electrophoretic mobility shift assays (EMSA) showed that activator protein 1 (AP-1) binding to a cognate AP-1 sequence was detected at 6 h and could be blocked by curcumin. Protein binding to the complete BZLF1 promoter ZIII site (ZIIIA+ZIIIB) demonstrated several specific complexes that gave weak signals at 6 h and 12 h but strong signals at 24 h, all of which were reduced after application of curcumin. Autostimulation of BZLF1 mRNA induction through binding to the ZIII site at 24 h was confirmed by antibody-induced supershift analysis. The present results confirm our previous finding that curcumin is an effective agent for inhibition of EBV reactivation in Raji DR-CAT cells (carrying DR-dependent chloramphenicol acetyltransferase), and they show for the first time that curcumin inhibits EBV reactivation mainly through inhibition of BZLF1 gene transcription. Copyright 2002 Wiley-Liss, Inc.
1: Am Surg. 1998 Jan;64(1):47-51; discussion 51-2.Links
The effect of curcumin on human B-cell immortalization by Epstein-Barr virus.Ranjan D, Siquijor A, Johnston TD, Wu G, Nagabhuskahn M.
Department of Surgery, University of Kentucky, Lexington, USA.
Cyclosporine is a commonly used immunosuppressant in solid-organ transplantation. It is, however, associated with an increased incidence of Epstein-Barr virus (EBV)induced post-transplant lymphoproliferative disorder (PTLD). In this study, human B lymphocytes isolated from healthy volunteers were immortalized in vitro with EBV. The effect of oxidative stress mediated by cyclosporine A or hydrogen peroxide on in vitro B cell immortalization was studied by coculturing immortalized B cells with cyclosporine A and hydrogen peroxide. Curcumin, a phenolic extract of the spice turmeric, was then used to observe its effect on this process. We found that in vitro B-cell immortalization with EBV was promoted by the oxidative stress induced by cyclosporine A and hydrogen peroxide, with the maximum effect seen at concentrations of 500 ng/ml and 100 microM, respectively. Curcumin blocked the B-cell immortalization in a dose-dependent fashion with nearly complete inhibition at 20 microM. We conclude that, because both hydrogen peroxide and cyclosporine A strongly promote in vitro B-cell immortalization with EBV (the putative process responsible for PTLD) and curcumin, an extract of a common spice is an effective inhibitor of this process; curcumin may be an effective adjunct in the prevention of PTLD in the patients undergoing therapy with cyclosporine A.
1: J Surg Res. 1999 Nov;87(1):1-5. Links
Enhanced apoptosis mediates inhibition of EBV-transformed lymphoblastoid cell line proliferation by curcumin.Ranjan D, Johnston TD, Reddy KS, Wu G, Bondada S, Chen C.
Department of Surgery, University of Kentucky, Lexington, Kentucky 40536, USA.
BACKGROUND: Epstein-Barr virus (EBV)-associated B-cell lymphomas occur more frequently in immunodeficient states such as organ transplantation and HIV infection. We have previously reported that B cell immortalization with EBV was promoted by cyclosporin A (CyA) and that curcumin (Cur), a natural phenol with known antioxidant and antitumor properties, blocked EBV-induced B cell immortalization. In the following experiments we show that Cur inhibits the proliferation of EBV-transformed lymphoblastoid cell lines (LCL) via enhanced apoptosis. METHODS: LCL were generated by infecting freshly isolated human B cells with EBV (B95-8) for 12 h and coculturing with predetermined optimal concentrations of CyA (500 ng/ml) for 4 weeks. LCL were then either frozen for future use or propagated for immediate experiments. These cells were then plated in 96-well plates with 20 microM Cur or 0.1% DMSO (vehicle control). The number of immortalized colonies/well, cell count, and (3)H uptake were used as an index of immortalization. To assess apoptosis rate LCL were cultured with 0.1% DMSO or Cur (20 microM) for 0, 18, and 42 h in culture flasks and then stained with MC540 and H33342, as markers for apoptosis, and analyzed by FACS. RESULTS: A profound inhibition of proliferation was seen in the LCL with 20 microM curcumin compared to 0.1% DMSO control. The colony count reduced from 34.5 +/- 3.4 to 0/well (P = 0.005), cell number reduced from 101,250 +/- 12,093 to 3750 +/- 1500/well (P = 0.002), and (3)H uptake reduced from 40,889 +/- 3669 to 70 +/- 5.2/well (P = 0.001). The apoptosis rate of LCL in the DMSO control at 24.07 and 16.87% increased significantly with 20 microM Cur to 76.4 and 95.1% at 18 and 42 h, respectively (P = 0.02). CONCLUSION: Cur is a potent inhibitor of EBV-transformed LCL. This effect appears to be mediated through enhanced apoptosis. A further investigation of this effect may be useful in prevention and therapy of B-cell lymphoma in immunodeficient patients. Copyright 1999 Academic Press.
1: J Nat Prod. 2003 Dec;66(12):1582-5. Links
Lucidenic acids P and Q, methyl lucidenate P, and other triterpenoids from the fungus Ganoderma lucidum and their inhibitory effects on Epstein-Barr virus activation.Iwatsuki K, Akihisa T, Tokuda H, Ukiya M, Oshikubo M, Kimura Y, Asano T, Nomura A, Nishino H.
K-Laboratories for Intelligent Medical Remote Services, 2266-22 Anagahora, Shimoshidami, Moriyama-ku, Nagoya 463-0003, Japan.
A new triterpene acid, lucidenic acid P (1a), and two new triterpene acid methyl esters, methyl lucidenates P (1b) and Q (2b), were isolated and characterized from the fruiting body of the fungus Ganoderma lucidum. Their structures were elucidated on the basis of spectroscopic methods. In addition, eight known triterpene acids, lucidenic acids A (3a), C (4a), D(2) (5a), E(2) (6a), and F (7a) and ganoderic acids E (9a), F (10a), and T-Q (11a), and six known triterpene acid methyl esters, methyl lucidenates A (3b), D(2) (5b), E(2) (6b), F (7b), and L (8b) and methyl ganoderate F (10b), were isolated and identified from the fungus. All of the triterpenoids, with the exception of 7a, were evaluated with respect to their inhibitory effects on the induction of Epstein-Barr virus early antigen (EBV-EA) by 12-O-tetradecanoylphorbol-13-acetate (TPA) in Raji cells, which is known to be a primary screening test for antitumor promoters. All of the compounds tested showed potent inhibitory effects on EBV-EA induction (96-100% inhibition at 1 x 10(3) mol ratio/TPA
1: Phytother Res. 2008 Feb;22(2):141-8. Links
Antiviral effects of Glycyrrhiza species.Fiore C, Eisenhut M, Krausse R, Ragazzi E, Pellati D, Armanini D, Bielenberg J.
Department of Medical and Surgical Sciences-Endocrinology, University of Padua, Padova, Italy.
Historical sources for the use of Glycyrrhiza species include ancient manuscripts from China, India and Greece. They all mention its use for symptoms of viral respiratory tract infections and hepatitis. Randomized controlled trials confirmed that the Glycyrrhiza glabra derived compound glycyrrhizin and its derivatives reduced hepatocellular damage in chronic hepatitis B and C. In hepatitis C virus-induced cirrhosis the risk of hepatocellular carcinoma was reduced. Animal studies demonstrated a reduction of mortality and viral activity in herpes simplex virus encephalitis and influenza A virus pneumonia. In vitro studies revealed antiviral activity against HIV-1, SARS related coronavirus, respiratory syncytial virus, arboviruses, vaccinia virus and vesicular stomatitis virus. Mechanisms for antiviral activity of Glycyrrhiza spp. include reduced transport to the membrane and sialylation of hepatitis B virus surface antigen, reduction of membrane fluidity leading to inhibition of fusion of the viral membrane of HIV-1 with the cell, induction of interferon gamma in T-cells, inhibition of phosphorylating enzymes in vesicular stomatitis virus infection and reduction of viral latency. Future research needs to explore the potency of compounds derived from licorice in prevention and treatment of influenza A virus pneumonia and as an adjuvant treatment in patients infected with HIV resistant to antiretroviral drugs.
1: Antiviral Res. 2003 Jun;59(1):41-7. Links
Mechanism of action of glycyrrhizic acid in inhibition of Epstein-Barr virus replication in vitro.Lin JC.
Department of Microbiology, College of Medicine, Tzu Chi University, 701 Section 3, Chung Yang Road, Hualien 970, Taiwan ROC. email@example.com
We report here that glycyrrhizic acid (GL), a component of licorice root (Glycyrrhiza radix), is active against EBV replication in superinfected Raji cells in a dose-dependent fashion. The IC(50) values for viral inhibition and cell growth were 0.04 and 4.8mM, respectively. The selectivity index (ratio of IC(50) for cell growth to IC(50) for viral DNA synthesis) was 120. Time of addition experiments suggested that GL interferes with an early step of EBV replication cycle (possibly penetration). GL had no effect on viral adsorption, nor did it inactivate EBV particles. Thus, GL represents a new class of anti-EBV compounds with a mode of action different from that of the nucleoside analogs that inhibit viral DNA polymerase
green tea 3g
1: Biochem Biophys Res Commun. 2003 Feb 21;301(4):1062-8. Links
Inhibition of Epstein-Barr virus lytic cycle by (-)-epigallocatechin gallate.Chang LK, Wei TT, Chiu YF, Tung CP, Chuang JY, Hung SK, Li C, Liu ST.
Department of Biology, Kaohsiung Medical University, 100, Shih-Chuan 1st Rd., 807, Kaohsiung, Taiwan.
(-)-Epigallocatechin gallate (EGCG), abundant in green tea, is a potent anti-microbial and anti-tumor compound. This investigation used immunoblot, flow cytometry, microarray, and indirect immunofluorescence analyses to show that at concentrations exceeding 50 microM, EGCG inhibits the expression of Epstein-Barr virus (EBV) lytic proteins, including Rta, Zta, and EA-D, but does not affect the expression of EBNA-1. Moreover, DNA microarray and transient transfection analyses demonstrated that EGCG blocks EBV lytic cycle by inhibiting the transcription of immediate-early genes, thus inhibiting the initiation of EBV lytic cascade.
1: Antiviral Res. 2006 Dec;72(3):171-7. Epub 2006 Jul 26. Links
Resveratrol inhibition of varicella-zoster virus replication in vitro.Docherty JJ, Sweet TJ, Bailey E, Faith SA, Booth T.
Northeastern Ohio Universities College of Medicine, P.O. Box 95, Rootstown, OH 44272, USA. firstname.lastname@example.org
Resveratrol was found to inhibit varicella-zoster virus (VZV) replication in a dose-dependent and reversible manner. This decrease in virus production in the presence of resveratrol was not caused by direct inactivation of VZV or inhibition of virus attachment to MRC-5 cells. The drug effectively limited VZV replication if added during the first 30 h of infection. Western blot analysis and real-time RT-PCR studies demonstrated that protein and mRNA levels of IE62, an essential immediate early viral protein, were reduced when compared to controls. These results demonstrate that VZV replication is adversely affected by resveratrol which is negatively impacting IE62 synthesis.
1: J Immunol. 2007 Jul 15;179(2):753-63. Links
Honokiol, a natural plant product, inhibits inflammatory signals and alleviates inflammatory arthritis.Munroe ME, Arbiser JL, Bishop GA.
Department of Microbiology, University of Iowa, IA 52242, USA.
Honokiol (HNK), a phenolic compound isolated and purified from magnolia, has been found to have a number of pharmacologic benefits, including anti-angiogenic and anti-inflammatory properties. HNK has long been used in traditional Asian medicine without toxic side effects. We and others have extensively studied signaling to B cells by CD40 and its Epstein Barr viral mimic, latent membrane protein 1 (LMP1), which has been implicated in exacerbation of chronic autoimmune disease. We asked whether HNK could inhibit CD40 and LMP1 inflammatory signaling mechanisms. In vivo, HNK stabilized the severity of symptomatic collagen-induced arthritis in both CD40-LMP1 transgenic mice and their congenic C57BL/6 counterparts. Ex vivo studies, including collagen-specific serum Ab and Ag recall responses, as well as CD40 or LMP1-mediated activation of splenic B cells, supported the anti-inflammatory effects of HNK. In mouse B cell lines expressing the human CD40-LMP1 chimeric receptor, CD40- and LMP1-mediated NF-kappaB and AP-1 activation were abrogated in a dose-dependent manner, with a concomitant decrease in TNF-alpha and IL-6. These promising findings suggest that the nontoxic anti-inflammatory properties of HNK could be valuable for blocking the autoimmune response.
1: Phytother Res. 2003 Jun;17(6):609-13. Links
Anti-herpesvirus activity of an extract of Ribes nigrum L.Suzutani T, Ogasawara M, Yoshida I, Azuma M, Knox YM.
Department of Microbiology, Asahikawa Medical College, 2-1-1-1 Midorigaoka-Higashi, Asahikawa 078-8510, Japan. email@example.com
An extract of Ribes nigrum L., known as blackcurrant in Europe and Kurokarin(R) in Japan, has been used as an ingredient in a variety of foods and folk medicine. In this study, the anti-herpesvirus activity of this extract was examined in vitro. The extract inhibited herpes simplex virus type 1 attachment on the cell membrane completely at a 100-fold dilution, as well as the plaque formation of herpes simplex virus types 1 and 2, and varicella-zoster virus by 50% at a 400-fold dilution or lower concentrations. This latter activity, which inhibits virus replication in cells, was due to the inhibition of protein synthesis in infected cells from the early stage of infection. Kurokarin is a possible candidate as a herbal medicine for herpesvirus infectious diseases. Copyright 2003 John Wiley & Sons, Ltd.