The percentage of subG1 population unfortunately was not determined during the analysis and the evaluation of this Kratom Ban Reversed population was qualitative. Kratom Ban Reversed mSE for 48 hr time period (Fig. MSE the cells in the G1 phase appeared to decrease but the overall profile was considerably altered.
Since in my present study the apoptotic-like cell death induced by MSE was suggested to be caspasesindependent an investigation looking at generation of ROS
in mediating the apoptotic events was carried out. Unfortunately the results in my study showed that there was no ROS generation upon kratom extract best treatment with high doses of MSE or MIT. During the ROS study another interesting observation was made specifically that MSE co-treatment with NAC appeared
to kratom liver toxicity protect the cells from death and that chemicals present in the MSE emphasised this effect.
I am always up for learning if there is anything to be learned. I have been combining my much mitragyna speciosa half life needed and legally prescribed amphetamine prescription with kratom for some time. I had been using kratom for years prior. I noticed the symptoms of dizziness and dehydration were a risk factor here but since kratom has made me only relaxed for years I have no overstimulation. Other people may react differently.
In the previous section it was noted that there were no major differences in p53 band intensity over the dose range tested compared to the control group implying that MIT does not induce the loss of protein as seen in the MSE treated cells. As with the p53 effects noted previously MIT had little effect on p21 levels (Fig. P21 levels of MSE treated SH-SY5Y cells at different time points (6 12 24 and 48 hr).
The control and low dose groups however did express p21 protein consistent with the p53 expression. In the parallel experiment with MIT again p21 was expressed in a time-dependant manner that correlated with p53 expression. MIT exerts weaker toxicity effects compared to MSE.
This assay was performed as instructed by the manufacturer Promega USA. Serial fluorescence readings were performed using a plate reader at 485 nm excitation and 520 nm emission. The SH-SY5Y cells were again used in this assay and the caspase inhibitors purchased from Calbiochem included Caspase-3 inhibitor II (Z-DEVD-FMK) Caspase-8 inhibitor II (Z-IETD-FMK) Caspase-9 inhibitor I (Z-LEHD-FMK) Caspase general inhibitor I (Z-VAD-FMK) negative control (Z-FA-FMK) and positive control doxorubicin HCL.