The p53 protein level was found to be decreased in a dose-dependant manner especially at kratom therapy white vein thai review lower concentrations of MSE treatment for 24 hr as shown in fig. Further experiments were carried out to determine the time course of the down regulation or loss of p53 (Fig. Worst Kratom Vendors mSE and control groups implying that this cell line expresses p53 protein and the lost of p53 protein seen at high doses was due to treatment effects.
The Arochlor 1254-induced rat liver S9 was a kind gift from Dr. Costas Ionnides of the University of Surrey U. The MLA assay protocols were obtained from the Genetic Toxicology Department of GlaxoSmithKline Company high on the hill kratom (Ware U –
- Dried leaves can also be chewed but since they are a bit tough most people prefer to crush them up or powder them first
- Vehicle treated control 0
- Parallel experiments were carried out to assess the effects of MIT on the expression of p21 protein
- Very good information is given in this blog about kratom extract
- M ketoconazole (KT) a CYP 3A4 inhibitor (Gibbs et al
. S9-mix for a treatment period of 24 hours. Selection of concentrations and preparation of test solutions The selection of concentration range tests was based on the cytotoxicity data using trypan blue exclusion assay performed as described in the previous chapter (Chapter 2).
The medium was replaced and the cells were treated again as before and returned to incubator. This process was repeated at 48 hrs. This is a homogeneous fluorometric method for estimating non-viable cells and also to estimate the total number of cells present in culture.
Prior to this study MIT was thought to be the compound responsible for the narcotic effects of this plant. In the early part of this study basic in vitro toxicology revealed that MSE and MIT have dose dependant toxicity to several human cell lines and the SH-SY5Y cell was the most sensitive. This is not surprising as the central nervous system was pharmacologically determined as the target system for the biological effects of this plant thus a toxicity
response might be anticipated in neuronal cells.
These reports confirm the complexity of maintenance of the cell cycle. HEK 293 MCL-5 and SH-SY5Y cells were used in this analysis. The cells were cultured and maintained as described in chapter
2 section 2. The chemicals for cell cycle analysis; propidium iodide RNase triton-x100 and ethyl alcohol absolute were purchased from Sigma-Aldrich (U. TEMED) from Bio-rad laboratories (Hemel Hempstead U. K); methanol from Fischer Scientific (U.
Measurement of cll-cylce phase-specific cell death using Hoechts 33342 and propidium iodide: Preservation by ethanol Worst Kratom Vendors fixation. The Journal of Histochemistry and Cytochemistry 36:1147-1152. Laboratory procedure for assessing specific locus mutations at the TK locus in cultured L5178Y mouse lymphoma kratom 120x extract harker heights cells.
Western culture is increasing and some individuals are now taking it for self-treatment in chronic pain and as an aid to opioid withdrawal (Boyer 2007). The potential toxicity of MSE and of other products derived from Mitragyna speciosa Korth is currently unknown. Therefore for the first time an in vitro toxicological assessment of this alkaloid extract (MSE) and its dominant alkaloid MIT has been examined. Both agents exerted dose-dependent cytotoxic effects to human cancer cells.
Tsuchiya et al 2002; Thongpradichote et al 1998; Tohda et al 1997). Thongpradichote et al 1998). PTX)-sensitive inhibitory G protein (Gi) (Tegeder et al 2003). Thus this information poses the question of whether the opioid receptors mediating the biological activity of the Mitragyna speciosa Korth plant may also mediate the MSE and MIT induced toxicity or cell death. I therefore predicted that opiate receptor antagonists would protect against MSE and MIT induced cell death.