2.Effect of Ankle States on Peak Torque of Knee Flexion and Extension for Old Adults
Zhixin NIU ; Qi ZHANG ; Qing YUE
Chinese Journal of Rehabilitation Theory and Practice 2012;18(7):610-611
Objective To explore the effect of state of the ankle on peak torque of knee flexors and extensors. Methods 18 adults in community over 65 years old were included. Their peak torque with knee flexion and extension was measured under 4 kinds of action of ankle. Results There was significant difference in peak torque neither flexion nor extension among 4 kinds of action of ankle (P>0.05). Conclusion It is unimportant of the state of ankle for knee training.
4.Scanning electron microscopic study on root canal cleaning effect using sodium hypochlorite at different temperatures
Qicheng LIU ; Weidong NIU ; Zhixin LIU ; Yang GU ; Xiandong YANG
Journal of Jilin University(Medicine Edition) 2006;0(02):-
Objective To assess the efficacy of NaClO irrigation of root canal at different temperatures.(Methods Thirty) human teeth with single root-canal mandible premolar were instrumented using standard technique,then were divided into 3 groups,carrying on root-canal irrigation.group A: 5.25% NaClO+System B,group B:5.25% NaClO+15% EDTA,group C:5.25% NaClO+System B+15% EDTA.After the teeth root were split,the scanning electron microscope was used to observe the coronal third,middle third and apical third parts.(Results The) amount of remaining debris on root canal wall in group C decreased significantly,compared with group A and B.The differences of coronal third and middle third between group A and B,group B and C,group A and C were significant(P0.05),but there were significant differences between group A,B and C(P
5.Exploration of Antidepressant Mechanism of Chaihu and Longgu Mulitang Based on cAMP/PKA/CREB/BDNF Signaling Pathway
Dike ZHAO ; Jun NIU ; Zhixin DU ; Chunyu ZHOU ; Shenao DING ; Xiaodan DU ; Liping YANG ; Mengdi MAO
Chinese Journal of Experimental Traditional Medical Formulae 2023;29(3):17-25
ObjectiveTo observe the intervention effect of Chaihu and Longgu Mulitang (CLMT) on rat depression model prepared by chronic unpredictable mild stress (CUMS) based on cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)/cAMP-response element-binding protein (CREB)-brain-derived neurotrophic factor (BDNF) signaling pathway. MethodSixty SD rats were divided into normal group, model group, and CLMT low-, medium- and high-dose groups and fluoxetine group (positive control) according to random number table. They, except the normal group, were treated with CUMS for 49 days to prepare the rat depression model. The CLMT low-, medium- and high-dose groups were given 2.89, 5.78 11.56 g·kg-1 of CHMD granules, respectively, and the fluoxetine group was given 2.06 mg·kg-1 of fluoxetine hydrochloride on the 29th day. The normal group and the model group received equal volume of normal saline for 21 days. The behavioral performance of rats were observed by open field test and forced swim test. The levels of 5-hydroxytryptamine (5-HT), norepinephrine (NE) and cAMP in rat hippocampus were measured by enzyme-linked immunosorbent assay (ELISA). The mRNA expressions of PKA, CREB, and BDNF in rat hippocampus were detected by real-time fluorescence quantitative polymerase chain reaction (Real-time PCR), and the protein expressions of PKA and BDNF were detected by Western blot. Immunohistochemistry was used to determine the expression of CREB, and hematoxylin and eosin (HE) staining and Nissl staining were used to observe the morphological changes of hippocampus. ResultCompared with the conditions in the normal group, the immobility time of the model group in the forced swim test was increased (P<0.01) and the total movement distance, residence time in central area, number of entries in central area and movement distance in central area were decreased (P<0.01). Additionally, the contents of 5-HT, NE and cAMP in hippocampus of the model group as well as the protein expressions of PKA, BDNF and CRE,the mRNA expressions of BDNF and CREB were lower than those in the normal group (P<0.01). Compared with the model group, the CLMT groups had reduced immobility time (P<0.01), elevated total movement distance, residence time in central area, number of entries in central area and movement distance in central area (P<0.05, P<0.01), up-regulated contents of 5-HT, NE and cAMP in hippocampus (P<0.05, P<0.01), and up-regulated protein expressions of PKA, BDNF and CREB and mRNA expressions of BDNF and CREB (P<0.01). HE staining and Nissl staining showed that CLMT significantly improved the neuronal structure in rat hippocampus. ConclusionCLMT alleviates the anxiety and depression of rats. These effects may be mediated by regulating monoamine neurotransmitters 5-HT and NE in hippocampus of depressed rats, activating cAMP/PKA/CREB/BDNF signaling pathway, up-regulating the expression of BDNF and protecting hippocampal structure and function .
6.LncRNA DACH1 protects against pulmonary fibrosis by binding to SRSF1 to suppress CTNNB1 accumulation.
Jian SUN ; Tongzhu JIN ; Zhihui NIU ; Jiayu GUO ; Yingying GUO ; Ruoxuan YANG ; Qianqian WANG ; Huiying GAO ; Yuhan ZHANG ; Tianyu LI ; Wenxin HE ; Zhixin LI ; Wenchao MA ; Wei SU ; Liangliang LI ; Xingxing FAN ; Hongli SHAN ; Haihai LIANG
Acta Pharmaceutica Sinica B 2022;12(9):3602-3617
Idiopathic pulmonary fibrosis (IPF) is a progressive disease with unknown etiology and limited therapeutic options. Activation of fibroblasts is a prominent feature of pulmonary fibrosis. Here we report that lncRNA DACH1 (dachshund homolog 1) is downregulated in the lungs of IPF patients and in an experimental mouse model of lung fibrosis. LncDACH1 knockout mice develop spontaneous pulmonary fibrosis, whereas overexpression of LncDACH1 attenuated TGF-β1-induced aberrant activation, collagen deposition and differentiation of mouse lung fibroblasts. Similarly, forced expression of LncDACH1 not only prevented bleomycin (BLM)-induced lung fibrosis, but also reversed established lung fibrosis in a BLM model. Mechanistically, LncDACH1 binding to the serine/arginine-rich splicing factor 1 (SRSF1) protein decreases its activity and inhibits the accumulation of Ctnnb1. Enhanced expression of SRSF1 blocked the anti-fibrotic effect of LncDACH1 in lung fibroblasts. Furthermore, loss of LncDACH1 promoted proliferation, differentiation, and extracellular matrix (ECM) deposition in mouse lung fibroblasts, whereas such effects were abolished by silencing of Ctnnb1. In addition, a conserved fragment of LncDACH1 alleviated hyperproliferation, ECM deposition and differentiation of MRC-5 cells driven by TGF-β1. Collectively, LncDACH1 inhibits lung fibrosis by interacting with SRSF1 to suppress CTNNB1 accumulation, suggesting that LncDACH1 might be a potential therapeutic target for pulmonary fibrosis.