Shenqi is a traditional Chinese polyherbal medicine has been widely used for the treatment of allergic rhinitis (AR). The aim of this study was to investigate the anti-allergic rhinitis activity of Shenqi and explore its underlying molecular mechanism. Ovalbumin (OVA)-induced allergic rhinitis rat model was used to evaluate the anti-allergic rhinitis effect of Shenqi. The effect of Shenqi on IgE-mediated degranulation was measured using rat basophilic leukemia (RBL-2H3) cells. Primary spleen lymphocytes were isolated to investigate the anti-allergic mechanism of Shenqi by detecting the expression of transcription factors via Western blot and the level of cytokines (IL-4 and IFN-γ) via ELISA. In OVA-induced AR rat models, Shenqi relieved the allergic rhinitis symptoms, inhibited the histopathological changes of nasal mucosa, and reduced the levels of IL-4 and IgE. The results from the in vitro study certified that Shenqi inhibited mast cell degranulation. Furthermore, the results of GATA3, T-bet, p-STAT6, and SOCS1 expression and production of IFN-γ and IL-4 demonstrated that Shenqi balanced the ratio of Th1/Th2 (IFN-γ/IL-4) in OVA-stimulated spleen lymphocytes. In conclusion, these results suggest that Shenqi exhibits an obvious anti-allergic effect by suppressing the mast cell-mediated allergic response and by improving the imbalance of Th1/Th2 ratio in allergic rhinitis.

Our study showed that SU monotherapy resulted in satisfactory glycemic control in most of the patients with NDM whose genetic defects are heterogeneous. The usage of SU may be considered as first-line therapy for patients with NDM in developing countries where effective genetic screening is not established.

The blood–brain barrier (BBB) and blood–nerve barrier ensure protection of the nervous system but pose a challenge for the treatment of pain since it restricts passage of many therapeutic drugs. Although it is unknown which blood–neural barrier is more relevant, or whether permeabilities are the same for different barriers, we proposed that the inefficiency of thiazolidinedione-type agonists for peroxisome proliferator-activated receptor gamma (PPARɣ) is due to their difficulty in passage through the BBB. We developed a new highly BBB penetrable PPARɣ agonist for the treatment of neuropathic pain, assuming BBB permeability is a rule of thumb to estimate the overall permeability of relevant blood–neural barriers.  As an index of brain penetration, the brain–plasma ratio (Kp) of ELB00824 is 5.13, suggesting very high brain bioavailability, which is 58-fold that of pioglitazone. The series of studies presented here indicate that ELB00824 may be the most potent PPARɣ agonist currently known for acute reduction of neuropathic pain in trigeminal nerve in rat and mouse models. Low-dose PPARɣ agonist, ELB00824 (10 mg/kg), effectively decreased neuropathic hypersensitivity in mice and rats at both acute and chronic time points, a dose 100-fold lower than the effective dose (1000 mg/kg, i.p.) of pioglitazone. Comparisons of ELB00824 alone or in combination with gabapentin or carbamazepine are provided. While PPARɣ agonists used to treat Type 2 diabetes produce several adverse side effects, sub-chronic oral toxicity study provided promising results that ELB00824 does not produce any significant short-term toxicity. The study animals of either sex remained alive and healthy with no significant alteration of body weight long term. Toxicity study results obtained were satisfactory, with no significant alterations in any serum biochemistry parameters.

No abstract

The aim of the present study was to longitudinally investigate the association of BDNF Val66Met with PTSD symptoms in Chinese Han adolescents who experienced the 2008 Wenchuan earthquake. Variants of BDNF Val66Met were identified by polymerase chain reaction-restriction fragment length polymorphism analyses and verified by DNA sequencing. PTSD symptoms were assessed by the PTSD Checklist-Civilian Version (PCL-C) among high school students at 6, 12, and 18 months after the earthquake. No differences of PTSD prevalence and PCL-C scores were found between the Val/Val homozygotes and the Met allele carriers at 6, 12, and 18 months after the earthquake regardless of gender. Decreased PTSD prevalence was observed at 12 and 18 months when compared with that at 6 months after the earthquake regardless of gender and the genotype. Meanwhile, PCL-C scores were decreased consecutively in the female subjects regardless of the genotypes. However, the scores at 18 months were lower when compared with those at 12 months in the male Val/Val homozygotes, but not in the male Met allele carriers. In addition, differences were found for the predictors of PCL-C scores and PTSD prevalence between the Val/Val homozygotes and the Met allele carriers during follow-up. These findings suggest that the association of BDNF Val66Met with PTSD is longitudinally different in Chinese Han adolescents after the 2008 Wenchuan earthquake. The Val allele may be associated with reduced PTSD severity in male adolescents in the later stage of PTSD rehabilitation during follow-up.

No abstract

Asiatic acid (AA) could attenuate ischemia/reperfusion induced myocardial apoptosis through upregulating the Akt/GSK-3β/HIF-1α pathway. HIF-3α is a negative regulator of HIF-1α, whose mRNA is a potential target of miR-1290. AA could upregulate miR-1290 in non-small-cell lung cancer A549 cells. This work aimed to investigate whether AA could inhibit hypoxia induced cardiomyocyte apoptosis through regulating the miR-1290/HIF3A/HIF-1α axis. The AC16 human myocardial cell line cultured under normoxic or hypoxic conditions was treated with various doses of AA for 24 h. Afterwards cell viability, apoptosis and the expression of miR-1290, HIF3A, and HIF1A were evaluated. Cells transfected with miR-1290 mimic or inhibitor were used to determine the role of miR-1290 in the anti-apoptosis effect of AA and the expression of HIF3A and HIF1A. Dual luciferase assay was performed to confirm miR-1290 targeting of HIF3A. HIF3A overexpression was achieved by transfection of HIF3A1 overexpressing lentivirus, and its effect on miR-1290 and AA-regulated survival of cardiomyocytes was evaluated. AA treatment protected cardiomyocytes from hypoxia-induced apoptosis and upregulated miR-1290 and HIF1A, but downregulated HIF3A under hypoxia. The protective effect of AA was abolished by miR-1290 knockdown, whereas enhanced by miR-1290 overexpression. In addition, miR-1290 knockdown increased HIF1A expression, but reduced HIF3A expression in cardiomyocytes. Dual luciferase assay confirmed miR-1290 direct targeting the 3' UTR of HIF3A. HIF3A overexpression counteracted the anti-apoptosis effect of AA or miR-1290. In conclusion, AA can protect cardiomyocytes against hypoxia-induced apoptosis through regulating the miR-1290/HIF3A/HIF-1α axis, and miR-1290 may be a potential target in the prevention of myocardial ischemia-reperfusion injury. © 2017 IUBMB Life, 69(9):660-667, 2017.

"Add-back" therapy, based on the GnRH-a dose, does not reduce the efficacy of using GNRH-a for the management of endometriosis. "Add-back" therapy reduced the occurrence of side effects that can occur with GnRH-a therapy alone, such as osteoporosis and menopausal syndrome. There were no statistically significant differences when comparing the effectiveness of a variety of "add-back" regimens to each other.