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Neuroglobin is an oxygen-binding heme protein expressed predominantly in the brain. Despite many years of research, the exact distribution and expression of neuroglobin in the neocortical development and under mild hypoxia stress still remain unclear. Therefore, we aim to explore the expression of neuroglobin during neocortex expansion and under mild hypoxia stress in vivo. We used Kunming mice to examine the expression of Ngb protein during neocortex expansion. In addition, we analyzed the density of Ngb-positive neural stem cells using the Image-Pro PLUS (v.6) computer software program (Media Cybernetics, Inc.). Our data indicated that the density of the neuroglobin-positive neurons in mice cerebral cortex displayed a downward trend after birth compared with high expression of neuroglobin in a prenatal period. Similarly, we identified that neurons were capable of ascending neuroglobin levels in response to mild hypoxic stress compared with the no intervention group. These findings suggest that neuroglobin behaves as a compensatory protein regulating oxygen provision in the process of neocortical development or under physiological hypoxia, further contributing to the discovery of novel therapeutic methods for neurological disorders, which is clinically important.

Objective. To systematically review whether the Kangai injection (KAI), which is commonly used traditional Chinese medicine, can improve the clinical efficacy of chemotherapy and relieve adverse reactions of chemotherapy in advanced colorectal cancer (CRC) patients. Methods. A comprehensive literature search was performed in three English and three Chinese electronic databases until March 2019. The literature was screened by EndNote X8 and data were analysed by RevMan5 and Stata12.0. Results. This meta-analysis consisted of twenty-eight studies, of which 2310 cases were reported. Among the 2310 cases, 1207 cases were treated with KAI combined with chemotherapy and 1103 cases were treated with chemotherapy alone. The results showed that KAI combined with chemotherapy significantly improved tumor response (Risk Ratio (RR) =1.32; 95% confidence interval (CI): 1.22-1.43; p p p p p p p p = 0.0004); increased immune function (CD3+: MD=6.34; 95% CI: 5.52-7.16; p < 0.00001, CD4+: MD=-5.99; 95% CI: 5.20-6.78; p < 0.00001; and CD4+/CD8+: MD=0.34; 95% CI: 0.14-0.54; p < 0.0009), and prolonged survival time (OR =1.77; 95% CI: 1.25-2.50; p = 0.001). Renal dysfunction caused by chemotherapy was not affected by KAI treatment (Odds Ratio (OR) =0.53; 95%IC: 0.25-1.12; p = 0.10). Conclusion. KAI can increase clinical effectiveness, improve quality of life, alleviate ADRs, and prolong survival time in advanced colorectal (CRC) patients receiving chemotherapy.

Objective. To systematically evaluate the efficacy of Xihuang pill (XHP) in breast cancer patients receiving chemotherapy. Methods. Three English and four Chinese databases were searched. Literature was screened using EndNote X7 and data were analyzed by Review Manager. Results. This review included 13 randomized clinical studies of 1272 patients. The results showed that XHP increased the tumor response [risk ratio (RR) = 2.91; 95% confidence interval (CI): 1.98-4.26] and improved Karnofsky performance score (KPS) for breast cancer patients receiving chemotherapy [RR = 4.96; 95% CI = 2.07-11.86]. In addition, XHP treatment significantly reduced chemotherapy-induced adverse events, including nausea and vomiting [RR = 0.50; 95% CI = 0.33-0.74], WBC reduction [RR = 0.71; 95% CI = 0.47-1.06], platelet reduction [RR = 0.53; 95% CI = 0.19-1.44], hemoglobin reduction [RR = 0.31; 95% CI = 0.19-0.52], and hepatic function damage [RR = 0.63; 95% CI = 0.35-1.11]. Conclusion. XHP combined with chemotherapy in comparison with chemotherapy alone could significantly enhance the tumor response, improve KPS, and alleviate toxicity induced by chemotherapy in breast cancer patients.

Objective. To systematically review the effect of invigorating Pi and detoxification (Jianpi Jiedu, (JPJD)) herbs in advanced colorectal cancer (CRC) patients receiving chemotherapy. Methods. Three English and four Chinese databases were searched. Literature was screened by EndNote X7 and data were analyzed by RevMan 5.2. Results. This review comprised 12 randomized clinical studies of 701 patients. The results showed that JPJD herbs improved the therapeutic effect on Chinese medicine symptoms [risk ratio (RR) = 1.59; 95% confidence interval (CI): 1.35~1.88] and Karnofsky performance score [RR = 2.07; 95% CI: 1.52~2.82] for advanced CRC patients receiving chemotherapy, lowered the Chinese medicine symptoms’ score [weighted mean difference = −2.44; 95% CI: −3.23~−1.64], reduced the incidence of nausea and vomiting [RR = 0.23; 95% CI: 0.11~0.49], improved platelet at toxicity grades III-IV [odds ratio = 0.29; 95% CI: 0.12~0.74] and I–IV [RR = 0.65; 95% CI: 0.51~0.82], and improved white blood cell at toxicity grades III-IV [RR = 0.37; 95% CI: 0.23~0.58] and I–IV [RR = 0.69; 95% CI: 0.60~0.79]. However, the results showed no significant effect on tumor response. Conclusion. JPJD herbs can improve quality of life, relieve symptoms, and reduce adverse events of advanced CRC patients receiving chemotherapy.

Objective. To investigate the effects of QKF on expression of amyloid-beta (Aβ), interleukin-1 beta (IL-1β), and glial fibrillary acidic protein (GFAP) using a rat model of AD.Materials and Methods. Fifty-six male Sprague-Dawley rats were randomly divided into seven groups (eight rats each): control group, sham-operated group, AD model group, groups of AD rats administered with low, medium, and high doses of QKF, and the donepezil group. AD was established by bilateral injection ofβ-amyloid (Aβ) 1–40 into the hippocampus. Two days after AD was established, drugs were administered by gavage. After 14 days of treatment, we used RT-PCR, Western blotting, and immunohistochemistry to measure the transcript expression and protein abundance of Aβ, IL-1β, and GFAP, and methenamine silver staining was used to detect amyloid protein particle deposition.Results. Compared to the control group, the rats from the AD model group showed significantly greater expression levels of Aβ, IL-1β, and GFAP. However, these differences in expression were abolished by treatment with QKF or donepezil.Conclusion. QKF possesses therapeutic potential against AD because it downregulated Aβ, IL-1β, and GFAP in the hippocampus of AD rats. Future studies should further examine the mechanisms through which QKF produces its effects and the consequences of long-term QKF administration.

Background. Yanghe decoction (YHD) has been used in the treatment of breast cancer for hundreds of years in Asia. However, the underlying mechanisms are currently unknown. The present study aims to evaluate the efficacy of YHD on antitumor and immune system enhancement in a 4T1 mouse breast cancer model and to clarify the antitumor mechanisms of YHD in breast cancer. Materials and Methods. The YHD was orally administrated for 2 weeks after inoculation. Tumor tissues were then removed, weighed, and homogenized. Flow cytometry was used to detect the number of Myeloid-Derived Suppressor Cells (MDSCs), Natural Killer T Cells (NKTs), and T cell subsets. Quantitative real-time PCR was used to detect the expression of inducible nitric oxide synthase (iNOS) and arginase-1 (ARG-1). Western blot was used to detect the protein expression of signal transducers and the activator of transcription 1 (STAT1), phosphorylated-signal transducers and the activator of transcription 1 (p-STAT1), signal transducers and the activator of transcription 3 (STAT3), and phosphorylated-signal transducers and the activator of transcription 3 (p-STAT3). The expression levels of interleukin-6 (IL-6), transforming growth factor-β (TGF-β), and interferon-γ (IFN-γ) were detected using an enzyme linked immunosorbent assay. Results. We found that the tumor weight of YHD high-dose group was significantly lower compared with the control group (pβ, and p-STAT3 and significantly increased the expression of IFN-γ, NKTs, CD4+ T cells, and p-STAT1. Conclusion. Our results showed that The mechanisms of YHD inhibit 4T1 breast tumor growth may be related to downregulating the expression of iNOS and ARG-1, negatively regulating the Janus kinase/STAT3 (JAK/STAT3) pathway by repressing the expression of IL-6 and TGF-β. Meanwhile, YHD enhances the immune capacity via increasing the expression of NKTs, CD4+ T cells, IFN-γ, and p-STAT1.