During a 5-20 d growth at moderate salinity (7 dS m‘i) in rice seedlings of salt sensitive cultivars Ratna and Jaya a larger decrease in chlorophyll (Chl) a and b contents was observed than in tolerant cvs. CSR-1 and CSR-3. At higher salinity (14 dS m'i) about 40 % declines in both whole chain electron transport and photosystem (PS) 2 activities were observed in the tolerant cvs. and about 62 to 67 % declines in the sensitive ones. No apparent change in PSI activity was observed due to salinization in the both sets of cultivars. Higher rate of Hill reaction was observed in chloroplasts ffom salt stressed seedlings of tolerant cultivars whereas inhibition in this activity was found in the sensitive ones. Chloroplasts isolated from stressed seedlings of sensitive cultivars showed about 31 % reduction in fluorescence emission at 685 nm as well as a major decrease in absorption with shifts in peaks in the visible region of spectrum. Thus salt sensitivity in rice is associated with decreased contents of Chls and carotenoids, PS2 and Hill reaction activities, and fluorescence emission.
Contractile dysfunction and fatal arrhythmias are the hallmarks of myocardial ischemia/reperfusion (I/R) injury. Pterostilbene has notable cardioprotective effects, but its main mechanisms are not fully understood. Here, we investigated the effect of PTE on myocardial hemodynamics, arrhythmias, inflammatory/oxidative responses, and the causal role of the JAK2/STAT3 pathway in rats with acute myocardial I/R injury. Sixty male 7-8 months Sprague-Dawley rats (n=10/each group) experienced in vivo model of myocardial I/R injury through 40-min LAD coronary artery occlusion and subsequent 24-h reperfusion. PTE at concentrations of 5 and 25 mg/kg was intraperitoneally administered to rats five min before reperfusion. Cardiac hemodynamics, reperfusion-induced ventricular arrhythmias, infarct size, inflammatory cytokines, oxidative stress markers, the activity of the JAK2/STAT3 pathway were measured as the endpoints. Administration of PTE to I/R-injured rats recovered myocardial contractile function and reduced infarct size and ventricular arrhythmias counts and incidence in a dosedependent manner. PTE at 25 mg/kg significantly and more potently reduced the levels of inflammatory mediators NF-κB, TNF-α, and IL-1β, suppressed intracellular ROS production, augmented the activity of glutathione, and manganesesuperoxide dismutase, and upregulated the JAK2 and STAT3 phosphorylation. Importantly, pretreatment of rats with Ag490 as a JAK2 inhibitor significantly abolished the cardioprotective and signaling effects of PTE in I/R rats. PTE exerts significant protective effects on reducing arrhythmias and myocardial infarction and enhancing cardiac function by stimulating JAK2/STAT3-related suppression of inflammatory and oxidative reactions in the I/R injury setting.