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BackgroundGlabrous rice, which lacks trichomes on the rice epidermis, is regarded as an important germplasm resource in rice breeding. Trichomes are derived from aerial epidermal cells and used as a model to study the cell fate determination in plant. In Arabidopsis, the molecular mechanisms of trichome development have been well studied. However, little is known about the molecular basis of trichome development in rice.ResultsIn this study, near isogenic lines harboring the glabrous rice 1 locus were developed. By a map-based approach, we narrowed down the locus to a 21-kb DNA region harboring two genes. One of the genes named Glabrous Rice 1 (GLR1), which is most likely the candidate, encodes a homeodomain protein containing the WOX motif. Constitutive Expression of GLR1 could partially complement the glabrous phenotype of NILglr1. The knock down of GLR1 by RNA interference led to a significant decrease in trichome number on the leaves and glumes of the RNAi transgenic plants.ConclusionGLR1 plays an important role in rice trichome development and will contribute to breeding of glabrous elite rice varieties.Electronic supplementary materialThe online version of this article (doi:10.1186/1939-8433-5-32) contains supplementary material, which is available to authorized users.

Inflammatory bowel disease (IBD) is a chronic, recurrent gastrointestinal inflammation that affects millions of people around the world. Loganin, an iridoid glycoside, has shown the anti‐inflammatory effects. However, the effect of loganin on IBD and its underlying molecular mechanism are not clear. The present study aimed to investigate whether loganin could alleviate IBD and its mechanisms. The intestinal epithelial Caco‐2 cell line was treated with lipopolysaccharide (LPS) to establish an in vitro IBD model. MTT assay was used to detect cell viability. The expression and release level of inflammatory factors were determined by both real‐time‐PCR and ELISA. Western blotting was used to assess the NF‐κB and JAK/STAT3 pathway‐related protein levels. The results showed that loganin repressed the expression and release of IL‐6, TNF‐α, and IL‐1β, and inhibited TLR4/NF‐κB and JAK/STAT3 signaling pathways in a concentration‐dependent manner. Overexpression of TLR4 could reverse the effect of loganin, leading to activation of NF‐κB signaling and production of inflammatory factors. Meanwhile, IGF‐1, a JAK/STAT3 signaling activator, could also reverse the anti‐inflammation effect of loganin. In conclusion, loganin inhibited LPS‐activated intestinal epithelial inflammation by repressing TLR4/NF‐κB and JAK/STAT3 signaling pathway.

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Clear cell renal cell carcinoma (ccRCC) is the most common malignant type of kidney cancer. This study aims to explore the underlying mechanism and potential targets of the traditional Chinese medicine Bu-Shen-Jian-Pi-Fang (BSJPF) in the treatment of ccRCC based on network pharmacology. After obtaining the complete composition information for BSJPF from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform, we analyzed its chemical composition and molecular targets and then established a pharmacological interaction network. Twenty-four significantly differentially expressed genes and 9 pathways mainly related to tumor proliferation were identified and screened. Functional enrichment analysis indicated that the potential targets might be significantly involved in glycolysis and the HIF-1 signaling pathway. To further confirm the effect of BSJPF on ccRCC cell proliferation, a BALB/c xenograft mouse model was constructed. Potential targets involved in regulating glycolysis and the tumor immune microenvironment were evaluated using RT-qPCR. VEGF-A expression levels were markedly decreased, and heparin binding-EGF expression was increased in the BSJPF group. BSJPF also inhibited tumor proliferation by enhancing GLUT1- and LDHA-related glycolysis and the expression of the immune checkpoint molecules PD-L1 and CTLA-4, thereby altering the immune-rejection status of the tumor microenvironment. In summary, this study demonstrated that the mechanism of BSJPF involves multiple targets and signaling pathways related to tumorigenesis and glycolysis metabolism in ccRCC. Our research provides a novel theoretical basis for the treatment of tumors with traditional Chinese medicine and new strategies for immunotherapy in ccRCC patients.