Aim Long non‐coding RNAs were widely reported to regulate laryngeal squamous cell carcinoma (LSCC), a prevalent tumor in the head and neck. We aimed to investigate the role of solute carrier organic anion transporter family member 4A1 antisense RNA 1 (SLCO4A1‐AS1) in LSCC. Materials & methods CCK‐8 and colony formation assays were conducted to examine the viability and proliferation of LSCC cells. The apoptosis of LSCC cells was evaluated using flow cytometry and TUNEL assays. The distribution of SLCO4A1‐AS1 in LSCC cells was detected by subcellular fractionation assay. The interaction between molecules was confirmed using luciferase reporter assay. Results SLCO4A1‐AS1 was overexpressed in LSCC tissues and cells. Furthermore, silenced SLCO4A1‐AS1 repressed the proliferation and facilitated apoptosis of LSCC cells. Mechanistical investigation revealed that SLCO4A1‐AS1 was a competing endogenous RNA (ceRNA) to upregulate SETD7 by binding with miR‐7855‐p. Additionally, SLCO4A1‐AS1 positively regulated the Wnt/β‐catenin signaling pathway by upregulating SETD7. Rescue experiments demonstrated that SLCO4A1‐AS1 promoted LSCC proliferation and inhibited LSCC apoptosis by upregulation of SETD7 and activation of the Wnt/β‐catenin pathway. Conclusion SLCO4A1‐AS1 promotes proliferation and inhibits apoptosis of LSCC cells by upregulation of SETD7 in a miR‐7855‐5p dependent way to activate the Wnt/β‐catenin pathway.
Objective. To conduct a systematic review on the mechanism of action and use of traditional Chinese medicines (TCM) in allergic rhinitis treatment. Background. Allergic rhinitis (AR) is a type I allergic disease of the immune system induced by immunoglobulin E mediated inflammation and is characterized by sneezing, nasal itching, paroxysmal nasal obstruction, mucosal edema, cough, and rhinorrhea. More than 500 million people have been affected by rhinitis worldwide in the past 20 years, leading to negative effects on health, quality of life, and social relationships. Currently, the trending medicines used in the case of AR include intranasal corticosteroids and oral H1 antihistamines, which are given as combinatorial medicines supplemented with immune therapy. These medications have been found to be very effective in either the short term or long term; however, they have been found to possess some serious side effects. Search Methodology. The information in this article on classical and traditional Chinese medications used to treat AR was derived from original papers and reviews published in Chinese and English language journals. Two Chinese databases (Wanfang and CNKI) and three English databases (Cochrane Library, PubMed, and Embase) were utilized for data gathering. Results. Traditional Chinese remedies have been identified to influence the production of cytokines such as IL-5 and IL-6, which are key mediators of eosinophilic inflammation, TNF-α, which stimulates TH2 cells at the site of inflammation, and NF-кB, which is required for cytokine and IgE antibody production. TCM has also been shown to be successful in lowering histamine levels, preserving histological changes by decreasing the thickness of the lamina propria, and downregulating the expression of Orai1, STIM1, and TRYC1, showing low expression of Ca+2 channel proteins. Conclusion. In this review, we discussed a series of classical, traditional Chinese medications, including Centipeda minima, Scutellaria baicalensis, licorice root (Glycyrrhiza uralensis), and others, as potential antiallergic agents and investigate their in vivo effect upon the production of cytokines and release of histamines for allergic rhinitis treatment.
Brain-derived neurotrophic factor (BDNF) regulates neuronal plasticity by targeting the tyrosine kinase B receptor (TrkB) receptor, but limited researches concentrate on the role of BDNF/TrkB signaling in vestibular compensation. In this study, rats with unilateral vestibular dysfunction were established by unilateral labyrinthectomy (UL) and infusion with siBDNF or 7, 8-Dihydroxyflavone (7,8-DHF, a TrkB receptor agonist). The behavioral scores of rats with vestibular deficits were determined and the rotarod test was performed after UL. BDNF and TrkB levels after UL were determined by western blot and quantitative reverse transcription PCR (qRT-PCR). 5-bromo-2ʹ-deoxyuridine (BrdU)-positive cells (newly generated cells) and GAD67-positive cells (GABAergic neurons) were identified by immunohistochemistry. Glial fibrillary acidic protein (GFAP) (astrocyte marker)-positive cells were identified and GABA type A receptor (GABA A R) expression was detected by immunofluorescence. We found that after UL, BDNF and TrkB levels were up-regulated with a maximum value at 4 h, and then progressively down-regulated during 4 h ~ 7 d. Blocking BDNF/TrkB signaling inhibited the recovery from vestibular deficits, decreased the numbers of newly generated cells and astrocytes in medial vestibular nucleus (MVN), inferior vestibular nerve (IVN), superior vestibular nerve (SVN) and lateral vestibular nucleus (LVN), and disrupted the balances of GABAergic neurons and GABA A R expressions in the left (lesioned) side and right (intact) side of MVN, whereas activation of BDNF/TrkB signaling caused opposite results. The current study indicated that BDNF/TrkB signaling avails vestibular compensation, depending on the number of newly generated cells and astrocytes, the rebalance of GABAergic neurons, and GABA A R expression in bilateral MVN.
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