Comparisons in phytochemical components and in vitro digestion properties of corresponding peels, flesh and seeds separated from two blueberry cultivars

Mei-Jia Li,Yuan-Yuan Deng,Li-Hua Pan,Shui-Zhong Luo,Zhizheng Jiang 한국식품과학회 2024 Food Science and Biotechnology Vol.33 No.1

Highbush blueberries (HB) and rabbiteye blueberries (RB) were separated into peels, flesh, and seeds to assess the compositions of nutriment, anthocyanins, soluble sugars and fatty acids, and the in vitro digesting abilities. Total phenolics contents (TPC) of 51–56 mg GAE/g DW were found in blueberry peels. Compared with HB peels, RB peels showed much higher TPC, but only contained 35 phenolics and lacked peonidin-3-O-rutinoside. Glucose, fructose, and sucrose were all present in HB and RB, but RB flesh had a higher acid-sugar ratio. Unsaturated fatty acid concentrations in HB and RB seeds were comparable (26.65 and 26.43 mg/g, respectively). However, HB seeds have 35 fatty acids, but RB seeds lacked cis-4,7,10,13,16,19-docosahexaenoic acid and cis-10-pentadecenoic acid. The in vitro digestion test showed that the whole fruit/peels/flesh of RB had a higher recovery and bioavailability index of phenolics and anthocyanins. Therefore, the reuse of blueberry pomace needs to be emphasized.

MiR-370-3p aggravates blood–brain barrier injury and neuron apoptosis by targeting SMURF1 to activate the TLR4/MyD88/NF-κB signaling in sepsis-associated encephalopathy

Wang Neng,Zhong Dan,Lin Jie,Ye Mei,Chen Yu,Wang Lili,Chen Mei,Luo Cong 대한독성 유전단백체 학회 2023 Molecular & cellular toxicology Vol.19 No.3

Background Sepsis-associated encephalopathy (SAE) is characterized by blood–brain barrier (BBB) disruption, neuron apoptosis and infl ammation. Studies show that miR-370-3p can be a new diagnostic biomarker for SAE. Objective This study aims to investigate the role of miR-370-3p in SAE and the underlying mechanism. Result An in vitro model of BBB disruption was established in brain microvascular endothelial cells (BMECs) with lipopolysaccharide (LPS). The expression level of RNAs was tested via RT-qPCR. Protein levels were detected by western blotting. Annexin V/PI double staining and CCK-8 assays were conducted to assess the apoptosis and viability of brain microvascular endothelial cells (BMECs). The migration of BMECs was detected by Transwell assay. BBB permeability analysis was performed to assess the relative permeability coeffi cient of BMECs. The in vitro barrier integrity was detected by trans-epithelial/ endothelial electrical resistance (TEER). The binding between miR-370-3p and SMAD specifi c E3 ubiquitin protein ligase 1 (SMURF1) was identifi ed by luciferase reporter assay. In this study, miR-370-3p was upregulated in LPS-treated BMECs. MiR-370-3p knockdown alleviated LPS-induced BBB disruption and apoptosis of BMECs, as well as recovered cell viability and migration. SMURF1 was directly targeted by miR-370-3p. SMURF1 silencing reversed the eff ects of miR-370-3p defi ciency in LPS-stimulated BMECs. Moreover, miR-370-3p activated the TLR4/MyD88/NF-κB signaling via regulating SMURF1 in LPS-stimulated BMECs. Conclusion MiR-370-3p aggravates BBB disruption and neuron apoptosis by targeting SMURF1 to activate the TLR4/ MyD88/NF-κB signaling in SAE.

Efficacy and safety of herbal medicine (Binafuxi granules) for the common cold with fever: A multicenter, randomized, double-blind, placebo-controlled, phase II clinical trial

Liu Xuemei,Min Jie,She Bin,Chen Yang,Li Jun,Huang Lei,Chen Ju,Luo Ai,Mei Yang,Li Ting,Wu Yanqing,Chen Daohong,Hongli Zhong,Liu Wei,Mao Bing,Jiang Hongli 한국한의학연구원 2023 Integrative Medicine Research Vol.12 No.3

Background: Binafuxi granules are a traditional Uighur medicine (TUM) for treating the common cold with fever. However, high-quality clinical studies supporting its efficacy and safety are lacking. Methods: In this multicenter, randomized, double-blind, placebo-controlled, phase II clinical trial, patients with common cold and fever were randomly assigned to a high-dose group, low-dose group, and placebo group in a 1:1:1 ratio. Outcomes were time to fever relief, time to fever clearance, proportion of afebrile patients, time to symptom disappearance, rate of symptom disappearance, effective rate, emergency drug usage and safety assessment. Results: A total of 235 patients were recruited. Of these, 234 were included in the full analysis set (FAS), and 217 were included in the per-protocol set (PPS). In the FAS analysis, the median time to fever relief was 6.00 h, 5.54 h and 10.65 h (P = 0.31) in the high-dose group, low-dose group and placebo group, respectively. The median time to fever clearance was 18.29 h, 20.08 h and 25.00 h (P = 0.0018), respectively, and the proportion of afebrile patients was 92.4%, 89.7% and 71.4% (P = 0.0002), respectively. There was a significant difference in the disappearance time and disappearance rate of all symptoms and of individual symptoms. No serious adverse events were found. Conclusions: Binafuxi granules can dose-dependently shorten the fever course and improve clinical symptoms in patients suffering from the common cold with fever.

Ischemic postconditioning protects cardiomyocytes against ischemia/reperfusion injury by inducing MIP2

Zhu, Hong-Lin,Wei, Xing,Qu, Shun-Lin,Zhang, Chi,Zuo, Xiao-Xia,Feng, Yan-Sheng,Luo, Qi,Chen, Guang-Wen,Liu, Mei-Dong,Jiang, Lei,Xiao, Xian-Zhong,Wang, Kang-Kai Korean Society for Biochemistry and Molecular Bion 2011 Experimental and molecular medicine Vol.43 No.8

Cardiomyocytes can resist ischemia/reperfusion(I/R) injury through ischemic postconditioning (IPoC) which is repetitive ischemia induced during the onset of reperfusion. Myocardial ischemic preconditioning up-regulated protein 2 (MIP2) is a member of the WD-40 family proteins, we previously showed that MIP2 was up-regulated during ischemic preconditioning (IPC). As IPC and IPoC engaged similar molecular mechanisms in cardioprotection, this study aimed to elucidate whether MIP2 was up-regulated during IPoC and contributed to IPoC-mediated protection against I/R injury. The experiment was conducted on two models, an $in$ $vivo$ open chest rat coronary artery occlusion model and an $in$ $vitro$ model with H9c2 myogenic cells. In both models, 3 groups were constituted and randomly designated as the sham, I/R and IPoC/hypoxia postconditioning (HPoC) groups. In the IPoC group, after 45 min of ischemia, hearts were allowed three cycles of reperfusion/ischemia phases (each of 30 s duration) followed by reperfusion. In the HPoC group, after 6 h of hypoxia, H9c2 cells were subjected to three cycles of 10 minute reoxygenation and 10 minute hypoxia followed by reoxygenation. IPoC significantly reduced the infarct size, plasma level of Lactate dehydrogenase and creatine kinase MB in rats. 12 h after the reperfusion, MIP2 mRNA levels in the IPoC group were 10 folds that of the sham group and 1.4 folds that of the I/R group. Increased expression of MIP2 mRNA and attenuation of apoptosis were similarly observed in the HPoC group in the $in$ $vitro$ model. These effects were blunted by transfection with MIP2 siRNA in the H9c2 cells. This study demonstrated that IPoC induced protection was associated with increased expression of MIP2. Both MIP2 overexpression and MIP2 suppression can influence the IPoC induced protection.

Ischemic postconditioning protects cardiomyocytes against ischemia/reperfusion injury by inducing MIP2

Hong-Lin Zhu,Kang-Kai Wang,Xing Wei,Shun-Lin Qu,Chi Zhang,Xiao-Xia Zuo,Yan-Sheng Feng,Qi Luo,Guang-Wen Chen,Mei-Dong Liu,Lei Jiang,Xian-Zhong Xiao 생화학분자생물학회 2011 Experimental and molecular medicine Vol.43 No.8

Cardiomyocytes can resist ischemia/reperfusion (I/R)injury through ischemic postconditioning (IPoC)which is repetitive ischemia induced during the onset of reperfusion. Myocardial ischemic preconditioning up-regulated protein 2 (MIP2) is a member of the WD-40family proteins, we previously showed that MIP2 was up-regulated during ischemic preconditioning (IPC). As IPC and IPoC engaged similar molecular mechanisms in cardioprotection, this study aimed to elucidate whether MIP2 was up-regulated during IPoC and contributed to IPoC-mediated protection against I/R injury. The experiment was conducted on two models,an in vivo open chest rat coronary artery occlusion model and an in vitro model with H9c2 myogenic cells. In both models, 3 groups were constituted and randomly designated as the sham, I/R and IPoC/hypoxia postconditioning (HPoC) groups. In the IPoC group, after 45 min of ischemia, hearts were allowed three cycles of reperfusion/ischemia phases (each of 30 s duration)followed by reperfusion. In the HPoC group, after 6 h of hypoxia, H9c2 cells were subjected to three cycles of 10 minute reoxygenation and 10 minute hypoxia followed by reoxygenation. IPoC significantly reduced the infarct size, plasma level of Lactate dehydrogenase and creatine kinase MB in rats. 12 h after the reperfusion,MIP2 mRNA levels in the IPoC group were 10 folds that of the sham group and 1.4 folds that of the I/R group. Increased expression of MIP2 mRNA and attenuation of apoptosis were similarly observed in the HPoC group in the in vitro model. These effects were blunted by transfection with MIP2 siRNA in the H9c2cells. This study demonstrated that IPoC induced protection was associated with increased expression of MIP2. Both MIP2 overexpression and MIP2 suppression can influence the IPoC induced protection.