Tropaeolum majus L. and low dose gamma radiation suppress liver carcinoma development via EGFR-HER2 signaling pathway.

Hepatocellular carcinoma (HCC) is one of the most fatal cancers around the world and remain asymptomatic in early stage. An alcoholic extract prepared from leaves of Tropaeolum majus L. (Tropaeolaceae) was assessed for its potential activity against diethylnitrosamine-induced liver carcinoma in vivo. Oral administration of the extract significantly decreased the inflammatory marker translation NF-kB and supressed HCC progression in combination with 0.5 Gy gamma radiation via EGF-HER-2 pathway. Histopathological and immunohistopathological features also showed the recovery of a hepatic architecture. Immunohistochemical study showed the T. majus and LDR enhancement effect on proapoptotic markers (caspase-3 and Bax) and inhibition of anti-apoptotic factor (BCl2). HPLC-DAD-MSn analysis of the extract revealed the annotation of twelve compounds. T. majus could mediate a defensive influence against diethylnitrosamine-induced hepatocarcinogenesis and serve as a respectable option in amelioration of the hepatocellular carcinoma development in combination with low dose of gamma radiation.

Chrysin attenuates global cerebral ischemic reperfusion injury via suppression of oxidative stress, inflammation and apoptosis.

Global cerebral ischemia is a leading cause of mortality worldwide. Several biomechanisms play a role in the pathology of cerebral ischemia reperfusion damage, such as oxidative stress, inflammation, apoptosis and excitotoxicity. Chrysin, a natural flavonoid with many important biological activities, was investigated in the present study for its possible neuroprotective properties in a rat model of global ischemia reperfusion. Male Wistar rats were allocated into three groups: sham-operated, ischemia/reperfusion, and chrysin (30 mg/kg) groups. All animals were subjected to ischemia for 15 min followed by reperfusion for 60 min, except for the sham-operated group. Rats were decapitated, then both hippocampi were rapidly excised to evaluate several biomarkers that reflect ischemic injury. The obtained results showed that pre-treatment with chrysin attenuated ischemia-induced oxidative stress by: (i) restoring the glutathione level; and (ii) depressing the levels/activities of thiobarbituric acid reactive substances, the hippocampal NADPH, as well as the xanthine oxidase. Exposure to chrysin also suppressed the inflammation accompanying the ischemia/reperfusion (I/R) damage, through increasing the interleukin-10 level, while decreasing the levels of both interleukin-6 and tumour necrosis factor-alpha. Moreover, an increase in Bcl2 and a decrease in both BAX and Hsp90 levels were recorded following chrysin exposure, which was also accompanied with elevated glutamate and aspartate levels. In conclusion, chrysin has demonstrated an anti-ischemic potential, through attenuation of the mechanisms underlying I/R injury. These data add to the knowledge on the significance of natural flavonoids as neuroprotective agents.