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Objective: To observe the clinical efficacy of the Zhuang medicine Yingbupu decoction on stage I and II acute kidney injury through sequential test. Methods: The open one-way qualitative response sequential design of experiments was adopted, and the patients with AKI in phase I and II who met the inclusion criteria were divided into the treatment group and the control group according to the order of hospitalization by random number table. On the basis of basic treatment, the treatment group was treated with Zhuang medicine Yingbupu decoction, and the control group was treated with Jinshuibao tablet. The clinical efficacy, TCM syndrome score, 24 h urine volume, serum creatinine (Scr), microalbumin in urine (mAlb), neutrophil Gelatinase related lipid delivery albumin (NGAL) of the two groups were compared, and the adverse reactions and complications of the two groups were observed. Results: After 14 d of treatment, when the treatment group reached the 10th case, the experimental line contacted the upper bound U-line and reached the experimental standard to terminate the experiment. The effective hypothesis was accepted, and it was believed that the Zhuang medicine Yingbupu decoction had a therapeutic effect on stage I and II AKI. The conclusion was drawn that the treatment group received the Zhuang medicine Yingbupu. The clinical effective rate and improvement days were similar between the two groups, and there was no significant difference (P>0.05). However, the integral value of traditional Chinese medicine syndrome in the treatment group was lower than that in the control group (P<0.05), After treatment, the Scr, mAlb, and NGAL levels of patients in both groups were lower than before treatment(P<0.05). After treatment, the Scr, mAlb, and NGAL values in the treatment group were significantly lower than those in the control group(P<0.05). After treatment, the 24-hour urine volume in both groups was higher than that before treatment, and the values in the treatment group were significantly higher than those in the control group (P<0.05). During the treatment period, there were no significant adverse reactions or complications in either group. Conclusion: The Zhuang medicine Yingbupu decoction is effective in treating stage I and II AKI, and the Zhuang medicine Yingbupu can significantly improve the symptoms and quality of life of patients with stage I and II AKI. Its improvement of renal function is better than that of Jinshuibao tablets, and its safety is good. [ABSTRACT FROM AUTHOR]

The specific mechanism of gingerol in cerebral ischemia remains unknown. A neuroprotective function for miR‐210 in cerebral ischemia has been identified. The brain‐derived neurotrophic factor (BDNF)‐mediated signaling pathway protects against cerebral ischemic injury. This investigation aimed to determine whether gingerol plays a neuroprotective role in cerebral ischemia via the miR‐210/BDNF axis. N2a cells subjected to 10 h of hypoxia and 4 h of reoxygenation were treated with 5, 10, or 20 μmol/L gingerol. The levels of viability, apoptosis, and proteins in N2a cells were determined using MTT assays, flow cytometry, and western blotting, respectively. The binding relationship between BDNF and miR‐210 was studied using a dual luciferase reporter assay. The expression levels of miR‐210 and BDNF were determined using qPCR. Gingerol repressed the increase in apoptosis and decrease in viability observed in response to hypoxia/reoxygenation. Gingerol increased Bcl‐2, BDNF, and TrkB levels and reduced Bax and cleaved caspase 3 levels after hypoxia/reoxygenation. Gingerol evoked decreased expression of miR‐210. Inhibition of miR‐210 resulted in increased viability and reduced apoptosis along with increased levels of Bcl‐2, BDNF, and TrkB and reduced levels of Bax and cleaved caspase 3 after hypoxia/reoxygenation. Additionally, the miR‐210 mimic reversed changes induced by gingerol. The cotransfection of the miR‐210 mimic and wild type BDNF led to decreased luciferase activity. BDNF was negatively regulated by miR‐210. BDNF siRNA reversed these changes evoked by miR‐210 inhibition. Gingerol ameliorated hypoxia/reoxygenation‐stimulated neuronal damage by regulating the miR‐210/BDNF axis, indicating that gingerol is worthy of further application in cerebral ischemia therapy. [ABSTRACT FROM AUTHOR]

Background: Recent investigations have suggested that long noncoding RNA (lncRNA) MIR22HG is commonly dysregulated in multiple types of malignancies. Nevertheless, the role of these MIR22HG in human colorectal carcinoma (CRC) are not well explored. Materials and Methods: Quantitative real-time polymerase chain reaction (qPCR) and in situ hybridization (ISH) assay were used to measure the expression of MIR22HG. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, and migration, as well as invasion assays, were utilized to determine the roles of MIR22HG on growth, apoptosis, migration, and invasiveness of CRC cell. The expression of E-cadherin and N-cadherin was measured using Western blotting and immunohistochemistry staining assay. CRC cell growth in vivo was analyzed using nude mice xenograft. Results: The qPCR and ISH assay revealed that MIR22HG was downregulated in CRC sample compared with in normal tissue. MIR22HG was also significantly downexpressed in CRC cells compared with that in normal colonic epithelial cell line. Overexpression of MIR22HG inhibited the growth, migration ability, and invasiveness of CRC cell in vitro. In addition, MIR22HG suppressed the epithelial-mesenchymal transition (EMT) and induced the apoptosis of human CRC cell. Moreover, the authors demonstrated that MIR22HG inhibited the tumor growth of CRC cell and regulated the expression of EMT markers (E-cadherin and N-cadherin) in vivo. Conclusion: Altogether, these results imply that lncRNA MIR22HG restrained the aggressive phenotypes of CRC cell. [ABSTRACT FROM AUTHOR]

Due to its extremely complex pathogenesis, no effective drugs to prevent, delay progression, or cure Alzheimer's disease (AD) exist at present. The main pathological features of AD are senile plaques composed of β-amyloid, neurofibrillary tangles formed by hyperphosphorylation of the tau protein, and degeneration or loss of neurons in the brain. Many risk factors associated with the onset of AD, including gene mutations, aging, traumatic brain injury, endocrine and cardiovascular diseases, education level, and obesity. Growing evidence points to chronic stress as one of the major risk factors for AD, as it can promote the onset and development of AD-related pathologies via a mechanism that is not well known. The use of murine stress models, including restraint, social isolation, noise, and unpredictable stress, has contributed to improving our understanding of the relationship between chronic stress and AD. This review summarizes the evidence derived from murine models on the pathological features associated with AD and the related molecular mechanisms induced by chronic stress. These results not only provide a retrospective interpretation for understanding the pathogenesis of AD, but also provide a window of opportunity for more effective preventive and identifying therapeutic strategies for stress-induced AD.