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In savin juniper, age and season can affect photosynthesis, chlorophyll fluorescence and photoprotective pigments. In spring, 2-year-old plants had more lutein than 5-year-olds, but the reverse occurred during summer and autumn. Savin juniper is an endemic evergreen shrub in the Mu Us Desert, where it establishes only with the protection of larger plants. Ultimately, established plants emerge into full sunlight as they grow. To explore how photoprotection responses change during this transition, a pot study was established under field conditions with three sunlight regimes (10%, 50% and 100% light transmittance) and two age cohorts (1- and 4-year-old rooted scions). To avoid potentially confounding effects of differences in leaf form, after one year we measured photosynthesis, chlorophyll fluorescence and foliar pigments of 2- and 5-year-old savin juniper on a monthly basis from April to October. For gas exchange and fluorescence variables, there were no interactions between cohort and sunlight except for intrinsic water-use efficiency in June; however, there were many interactions regarding pigment concentrations and ratios. Generally, 5-year-old plants had higher mean chlorophyll, total carotenoids, and chlorophyll a/b ratios than 2-year-old plants, but lower mean β-carotene/α-carotene ratio, zeaxanthin and lutein. Plants under brighter light had lower mean lutein. There were obvious changes in β-carotene/α-carotene, zeaxanthin and lutein in June, July and August, respectively. Under 100% sunlight, lutein concentration was higher in 2-year-old than 5-year-old plants from April to June, but this pattern reversed from July to October. The effects of age and season, in addition to the prevailing light regime, need to be considered when investigating the role of carotenoids in photoprotection.

Viral myocarditis is a common cardiovascular disease, which seriously endangers the health of people and even leads to sudden unexpected death. MicroRNAs play very important roles in various physical and pathological processes including cardiogenesis and heart diseases. In recent years, miR-20b has been implicated in various diseases such as breast cancer, gastric cancer, hepatocellular carcinoma, cardiovascular diseases. However, the function of miR-20b in the pathological progress of viral myocarditis has not been reported. In this study, we found that miR-20b was up-regulated in mouse heart tissues post Coxsackievirus B3 (CVB3) infection. Bioinformatics analysis identified ZFP-148, a transcription factor that plays essential roles in the regulation of virus replication, is one of the predicted targets of miR-20b. MiR-20b expression was found to be up-regulated and ZFP-148 protein level was markedly repressed during viral myocarditis. Further studies demonstrated that miR-20b directly binds to the 3'-UTR of ZFP-148 and suppresses its translation. Moreover, aberrant expression of miR-20b promoted the expression of anti-apoptosis proteins Bcl-2 and Bcl-xL, suggesting that altered gene expression might promote cardiomyocytes survival in viral myocarditis. Our findings indicated that miR-20b might be a potential therapeutic target for CVB3-induced viral myocarditis and a useful marker for the diagnosis of viral myocarditis.

Intracerebral hemorrhage (ICH) results in inflammation, and glucocorticoids have been proven to be effective inhibitors of ICH‑induced inflammation. However, the precise underlying mechanisms of ICH‑induced inflammation and glucocorticoid function remain largely undefined. Using a mouse ICH model, the present study demonstrated that the short non‑coding RNA molecule microRNA‑155 (miR‑155) is involved in the inflammatory process initiated by ICH in mice. Increased mRNA expression levels of miR‑155, as well as the pro‑inflammatory cytokines interferon‑β (IFN‑β), tumor necrosis factor‑α (TNF‑α) and interleukin‑6 (IL‑6), were observed in vivo following ICH. By contrast, the expression level of suppressor of cytokine signaling 1 (SOCS‑1) protein was reduced in the ICH group compared with control mice. Similar results were observed in vitro using astrocytes, the primary effector cells in ICH. Compared with wild type astrocytes, astrocytes overexpressing miR‑155 exhibited significant inhibition of SOCS‑1 protein expression levels. These results suggest that miR‑155 contributes to the development of ICH‑induced inflammation in mice by downregulating SOCS‑1 protein expression levels and promoting pro‑inflammatory cytokine (IFN‑β, TNF‑α and IL‑6) production. Expression levels of miR‑155 and pro‑inflammatory cytokines in the ICH group were significantly decreased following dexamethasone administration. This suggests that glucocorticoids attenuate ICH‑induced inflammation by targeting the miR‑155/SOCS‑1 signaling pathway in mice. In conclusion, the results of the present study demonstrated that the miR‑155/SOCS‑1 signaling pathway is required for ICH‑induced inflammation, and glucocorticoids inhibit this process by targeting the miR‑155/SOCS‑1 signaling pathway.