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AIM: To examine the effects of borneol on inflammation and myocardial remodeling after myocardial infarction (MI) in mice, and to investigate the underlying mechanisms. METHODS: Eight-week-old wild-type (WT) C57BL/6 mice and transient receptor potential cation channel subfamily M member 8 (TRPM8) gene knockout ( TRPM8-/-) mice were randomly divided into sham and MI groups, and were subsequently treated with normal saline (control group) or borneol (borneol group) via gavage. Survival curves were plotted for WT and TRPM8mice with MI treated with or without borneol. After 28 d, cardiac function of the mice was assessed through echocardiography, and haemodynamic indexes were evaluated using a multi-channel physiological instrument. Infarct size, myocardial hypertrophy and interstitial fibrosis were assessed via pathological staining. In addition, inflammatory response in the peri-infarct region was detected. RESULTS: The TRPM8 expression was up-regulated in the peri-infarct region of the mice with MI (P<0. 05), and borneol had no effect on TRPM8 expression (P>0. 05). Borneol increased the survival rate, reduced the infarct size, inhibited cardiac remodeling and improved cardiac function in WT mice with MI (P<0. 05 or P<0. 01). However, it did not affect the survival rate, infarct size, myocardial hypertrophy, myocardial fibrosis or cardiac function in TRPM8mice (P>0. 05). Furthermore, borneol reduced inflammatory cell infiltration and the expression of inflammatory cytokines, tumor necrosis factor-α (TNF-α ), interleukin-1β (IL-1β), IL-6 and monocyte chemotactic protein-1 (MCP-1), in WT mice (P<0. 05 or P<0. 01) but not in TRPM8-/- mice (P>0. 05). CONCLUSION: Borneol attenuates inflammation, inhibits cardiac remodeling and improves cardiac function in mice with MI via TRPM8. [ABSTRACT FROM AUTHOR]

Age-related macular degeneration (AMD) is a chronic disease, which progresses slowly from early to late stages over many years. Inflammation critically contributes to the pathogenesis of AMD. Here, we investigated the therapeutic potential of minocycline in a chronic model of AMD (i.e., the LysMCre-Socs3fl/flCx3cr1gfp/gfp double knockout [DKO] mice). Five-month-old DKO and wild type (WT) (Socs3fl/fl) mice were gavage fed with minocycline (25 mg/kg daily) or vehicle (distilled water) for 3 months. At the end of the treatment, visual function and retinal changes were examined clinically (using electroretinography, fundus photograph and optic coherence tomography) and immunohistologically. Three months of minocycline treatment did not affect the body weight, behaviour and general health of WT and DKO mice. Minocycline treatment enhanced the a-/b-wave aptitudes and increased retinal thickness in both WT and DKO. DKO mouse retina expressed higher levels of Il1b, CD68 and CD86 and had mild microglial activation, and decreased numbers of arrestin+ photoreceptors, PKCα+ and secretagogin+ bipolar cells compared to WT mouse retina. Minocycline treatment reduced microglial activation and rescued retinal neuronal loss in DKO mice. Our results suggest that long-term minocycline treatment is safe and effective in controlling microglial activation and preserving visual function in chronic models of AMD. [ABSTRACT FROM AUTHOR]

Circular RNAs (circRNAs) are a distinctive family of ncRNAs, and they function as key regulators in the initiation, development and progression of various diseases. However, the regulatory roles of circRNAs in the tumorigenesis of cervical cancer (CC) have not been fully understood. In this study, we identified a set of circRNAs in CC and paired normal tissues, using RNA sequencing data, and found that the cancer and normal tissues could be told apart by those differentially expressed (DE) circRNAs, indicating that circRNA expression profiles in CC were significantly different from those in the normal tissues. Meanwhile, the upregulated genes in CC were enriched in inflammation-related pathways, and the correlation analysis between the DE circRNAs and genes revealed that the abundance of DE circRNAs was positively related to the expression of their host genes. However, the expression of TGFBR2 and KDM4C were found to exhibit a negative correlation with their corresponding circRNAs. Furthermore, we also predicted the interactions between circRNAs and proteins, and constructed a competing endogenous RNA (ceRNA) network. Specifically, hsa_circ_0001495 was predicted to interact with ESRP2, and acted as a sponge by competing for miRNAs with TBL1XR1. Functionally, hsa_circ_0001495 was predicted to regulate epithelial cell proliferation and NOTCH signaling via ESRP2 and TBL1XR1, respectively. We also evaluated the prognostic values of downstream target genes of selected circRNAs, using clinical records of CC patients. In summary, the present study provided some regulatory circRNAs involved in CC tumorigenesis based on bioinformatics approaches, which brought strong evidences for researchers to further explore their biological and clinical values. • RNA sequencing data are employed to identify the circRNAs in CC and normal tissues. • CCs have significantly different circRNA expression profiles from the normal tissues. • TGFBR2 and KDM4C have negative correlation with their corresponding circRNAs. • Hsa_circ_0001495 is predicted to regulate ESRP2 and TBL1XR1. • Hsa_circ_0080414 may regulate genes involved in the normal function in cervix. [ABSTRACT FROM AUTHOR]

[Display omitted] • Cellulose nonwoven prepares the super-absorbent nonwoven by in-situ modification. • Electrospinning builds water channels in the hydrophobic layer of the dressing. • Self-pumping dressing offers unidirectional fluid transportation and moist healing. • The self-pumping dressing accelerates diabetic wound healing. The improper management of wound exudate around the diabetic wound bed is one of the major factors leading to delay diabetic wound healing. However, the limited water absorption of single-layer conventional dressings unavoidably maintains excessive exudate in the diabetic wound bed. Herein, a novel diabetic wound dressing is reported for achieving rapid wound healing by electrospinning hydrophobic nanofibers on a hydrophilic modified non-woven fabric. The double-layer structure of the self-pumping dressing possesses unidirectional fluid transportation to divert excessive exudate away from diabetic wounds, ultimately promoting wound healing. The hydrophilic modified non-woven fabric provides water absorption and moisture retention to absorb excess exudate passing through the hydrophobic nanofiber, thereby preventing the wound bed from rewetting. Moreover, the formation of depressions on the hydrophobic nanofiber surfaces serves as water channels to further drain wound exudate from the wound bed. In vivo wound studies confirm that the self-pumping dressing exhibits excellent unidirectional wound exudate delivery and wound moisturization. Thus, diabetic wound healing shows a low inflammatory response and excellent wound healing quality. This self-pumping dressing exhibits clinical significance to design and fabricate a next-generation dressing for diabetic wound healing. [ABSTRACT FROM AUTHOR]