Albiflorin relieves cerebral ischemia-reperfusion injury by activating Nrf2/HO-1 pathway.

Our work aims to investigate the functions of a natural compound, Albiflorin (AF) in cerebral ischemia-reperfusion (IR) injury. The cerebral IR models were established by OGD/R in PC12 cells and MCAO/IR in rats. The cells in a glucose-free medium were placed in an anaerobic chamber containing 95% N2 and 5% CO2 for 3h at 37°C, returned to a normal medium, and incubated for 24h to accomplish OGD/R. Focal cerebral ischemia was conducted by thread occlusion of the right middle cerebral artery for 2h followed by 24h reperfusion in rats. CCK-8 assay indicated that AF had no toxicity to PC12 cells. Flow cytometry, Western blot, or TUNEL showed that AF treatment reduced apoptosis of cells or rat brain tissues. qRT-PCR and ELISA showed that AF decreased IL-1ß, IL-6, and TNF-α levels in vitro and in vivo. Elevated levels of MDA, SOD, and ROS induced by IR injury were mitigated by AF in vitro and in vivo. HE and TTC staining revealed that AF ameliorated pathological injury in MCAO/IR rats. Western blot showed that Nrf2, NQO1, and HO-1 expression was activated by AF, and ML385 treatment suppressed the inhibition effects of AF in cerebral IR injury models. Overall, AF alleviates cerebral IR injury via regulating the Nrf2/HO-1 pathway.

LncRNA ITSN1-2 knockdown inhibits OGD/R-induced inflammation and apoptosis in mouse hippocampal neurons via sponging miR-195-5p.

OBJECTIVE: The upregulation of long noncoding RNA intersectin 1-2 (lnc ITSN1-2) is associated with poor prognosis in acute ischemic stroke (AIS) patients, but the role and mechanism of lnc ITSN1-2 in AIS are rarely reported, which, thus, are highlighted in this study. METHODS: AIS cell model was constructed by oxygen glucose deprivation and reoxygenation (OGD/R). The quantitative real-time PCR was used to detect the expression of lnc ITSN1-2 in HT22 cells. The effects of lnc ITSN1-2 overexpression or knockdown on viability, LDH release, apoptosis, inflammatory and apoptotic factor expressions in OGD/R-induced HT22 cells were measured by cell counting kit-8 assay, LDH release kit, flow cytometry, ELISA and western blot, respectively. Starbase was used to screen the target genes of lnc ITSN1-2. The targeting relationship between lnc ITSN1-2 and miR-195-5p was predicted by starbase and verified by dual-luciferase report assay. The above assays were conducted again to study the function of miR-195-5p. Lastly, the levels of activated mitogen-activated protein kinases (MAPK) pathway-related proteins were determined by western blot. RESULTS: OGD/R treatment reduced the HT22 cell viability and enhanced LDH release rate and lnc ITSN1-2 expression. Lnc ITSN1-2 overexpression promoted the cell injury, apoptosis and inflammation in OGD/R-induced HT22 cells, while lnc ITSN1-2 knockdown generated the opposite effect and deactivated the MAPK pathways. However, the effect of lnc ITSN1-2 knockdown in OGD/R-induced HT22 cells was reversed by miR-195-5p inhibitor. CONCLUSION: Lnc ITSN1-2 knockdown suppressed the inflammation and apoptosis in OGD/R-induced HT22 cells by regulating the miR-195-5p-mediated MAPK pathways.

Dynamic analysis of oral Candida carriage, distribution, and antifungal susceptibility in HIV-infected patients during the first year of highly active antiretroviral therapy in Guangxi, China.

BACKGROUND: Highly active antiretroviral therapy (HAART) as an effective therapy for immune reconstruction among patients with HIV/AIDS might have influence on oral Candida status. We investigated oral Candida carriage, distribution, and antifungal susceptibility dynamically during the first year of HAART among adult HIV-infected patients in Guangxi, China. METHODS: Forty-five adult HIV-infected patients who received their first year HAART in the AIDS clinic of the Guangxi Center for Disease Control (CDC) and 31 healthy individuals were recruited. Clinical information and oral examinations were obtained. Oral rinses taken from patients at baseline, 3, 6, 12 months during HAART, respectively, were cultured, and Candida species were identified following standard microbiological techniques. In vitro antifungal susceptibilities were tested by the broth microdilution method. RESULTS: The oral Candida load decreased gradually in the 45 patients with HIV/AIDS during the first year of HAART (P < 0.050). Among 176 Candida isolates, Candida albicans (114/176) was the predominant species, and Candida parapsilosis (23/62) was the most common non-albicans species. We found the frequency of resistance to fluconazole and itraconazole of Candida isolated from our samples increased (P < 0.05) after 12 months of HAART. In addition, the frequency of C. albicans isolates resistant to fluconazole and itraconazole was on the rise (P < 0.05). CONCLUSIONS: The Candida load decreased with increased CD4(+) T cell counts, and C. albicans was still the prevailing species. Further, a trend toward more frequent in vitro resistance to fluconazole and itraconazole was observed. Our results provide reference for treatment and prevention of oral candidiasis among this population.