The influence of low-temperature conditioning (LTC) treatment on chilling injury, glycine betaine content, and energy metabolism in loquat fruit at 1 °C storage was investigated. The results indicated that LTC treatment significantly reduced chilling injury index, ion leakage, and malondialdehyde content in loquat fruit. Betaine aldehyde hydrogenase (BADH) activity and endogenous glycine betaine (GB) content in loquats treated with LTC were significantly higher than those in control fruit. Moreover, LTC treatment induced activities of energy metabolism-associated enzymes, including H(+)-adenosine triphosphatase, Ca(2+)-adenosine triphosphatase, succinic dehydrogenase, and cytochrome c oxidase. LTC treatment triggered obviously higher levels of adenosine triphosphate (ATP) content and energy charge in loquat fruit. These results showed that LTC possibly alleviated chilling injury and enhanced chilling tolerance of loquat fruit by enhancing endogenous GB content and energy status.
In this letter, dual-band trapping of spoof surface plasmon polaritons (SSPPs) is realized by a simple surface plasmon waveguide (SPW), which takes the form of a microstrip line with periodic holes. A tapered microstrip line with periodic gradient holes is built for efficient mode conversion between the quasi-transverse electromagnetic waves in the common microstrip line and the SSPPs on the SPW. It is interesting to note that negative group velocity can be clearly observed on the first high-order mode of such SPW due to the strong coupling between the corrugated microstrip line and ground. A curved SPW of the same form is also investigated for testing its field confinement and circuitry function. Measurement results agree quite well with the simulation ones, which indicate this SPW can find potential applications in plasmonic integrated circuits at microwave and terahertz frequencies.
AIM: To investigate the role of the hydrogen-rich water (HRW) in the prevention of aspirin-induced gastric mucosal injury in rats. METHODS: Forty male rats were allocated into four groups: normal control group, HRW group, aspirin group, and HRW plus aspirin group. The protective efficacy was tested by determining the gastric mucosal damage score. Malondialdehyde (MDA), superoxide dismutase (SOD), myeloperoxidase (MPO), interleukin (IL)-06 and tumor necrosis factor (TNF)-α in gastric tissues were evaluated. The serum levels of IL-1β and TNF-α were also detected. Histopathology of gastric tissues and localization of Cyclooxygenase 2 (COX-2) were detected using hematoxylin and eosin staining and immunohistochemistry, respectively. RESULTS: Pretreatment with HRW obviously reduced aspirin-induced gastric damage scores (4.04 ± 0.492 vs 2.10 ± 0.437, P < 0.05). The oxidative stress levels of MDA and MPO in the gastric tissues increased significantly in the aspirin-treated group compared with the HRW group (2.43 ± 0.145 vs 1.79 ± 0.116 nmol/mg prot, P < 0.05 and 2.53 ± 0.238 vs 1.40 ± 0.208 U/g tissue, P < 0.05, respectively). HRW could obviously elevated the SOD levels in the gastric tissues (37.94 ± 8.44 vs 59.55 ± 9.02 nmol/mg prot, P < 0.05). Pretreatment with HRW significantly reduced IL-06 and TNF-α in the gastric tissues (46.65 ± 5.50 vs 32.15 ± 4.83 pg/mg, P < 0.05 and 1305.08 ± 101.23 vs 855.96 ± 93.22 pg/mg, P < 0.05), and IL-1β and TNF-α in the serum (505.38 ± 32.97 vs 343.37 ± 25.09 pg/mL, P < 0.05 and 264.53 ± 28.63 vs 114.96 ± 21.79 pg/mL, P < 0.05) compared to treatment with aspirin alone. HRW could significantly decrease the COX-2 expression in the gastric tissues (staining score: 8.4 ± 2.1 vs 2.9 ± 1.5, P < 0.05). CONCLUSION: HRW pretreatment alleviated the aspirin-induced gastric lesions by inhibiting the oxidative stress, inflammatory reaction and reducing the COX-2 in the gastric tissues.
Nitrogen dioxide (NO(2))-induced responses in wild type (wt) and salicylic acid (SA)-altering Arabidopsis mutants snc1 (suppressor of npr1-1, constitutive) with high SA level, transgenic line nahG with low SA level, npr1-1 (nonexpressor of PR gene) with SA signaling blockage and double mutant snc1nahG plants, were investigated. All mutant lines except sncl showed that NO(2) exposure at 0.25 microL L(-1) increased chlorophyll content and biomass accumulation, elevated photosynthetic rate, and decreased MDA content compared to their respective controls. The sncl plants were similar to the control plants for these measured indices. NO(2) exposure at 0.5 microL L(-1) and higher doses caused injury to wt, nahG, npr1-1 and snc1nahG plants, whereas the snc1 plants exhibited a stronger tolerance. To evaluate the resistance mechanism, we further investigated the changes in the mutants exposed to 1 microL L(-1) of NO(2) in relation to endogenous SA level, antioxidant capacity and redox status. The collected data demonstrated that the NO(2) tolerance in snc1, with a high SA level, was tightly linked to the increased antioxidant capacity and decreased oxidative stress. This suggests that SA may play an important protective function in plant response to NO(2) stress.
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