Effect of bamboo shoot dietary fiber on gel properties, microstructure and water distribution of pork meat batters.

OBJECTIVE: To develop healthier comminuted meat products to meet consumer demand, the gel properties, rheological properties, microstructure and water distribution of pork meat batters formulated with various amounts of bamboo shoot dietary fiber (BSDF) were investigated. METHODS: Different levels of BSDF (0% to 4%) were added to pork batters, and the pH, color, water-holding capacity, texture and rheological properties of pork batters were determined. Then, pork batters were analyzed for their microstructure and water distribution using scanning electron microscopy (SEM) and low-field nuclear magnetic resonance (LF-NMR). RESULTS: Compared with the control, BSDF addition into meat batters showed a significant reduction in L*-value and a significant increase in b*-value (p<0.05). BSDF addition of up to 4% reduced the pH value of pork batters by approximately 0.15 units; however, the cooking loss and expressible water loss decreased significantly (p<0.05) with the increased addition of BSDF. The hardness and gel strength were noticeably enhanced (p<0.05) as the content of BSDF increased. The rheological results showed that BSDF added into pork batters produced higher storage modulus (G') and loss modulus (G″) values. The SEM images suggested that the addition of BSDF could promote pork batters to form a more uniform and compact microstructure. The proportion of immobilized water increased significantly (p<0.05), while the population of free water was decreased (p<0.05), indicating that BSDF improved the water-holding capability of pork batters by decreasing the fraction of free water. CONCLUSION: BSDF could improve the gel properties, rheological properties and water distribution of pork meat batters and decrease the proportion of free water, suggesting that BSDF has great potential as an effective binder in comminuted meat products.

Comparative study of thermal gelation properties and molecular forces of actomyosin extracted from normal and pale, soft and exudative-like chicken breast meat.

OBJECTIVE: The objectives of this study were to investigate the thermal gelation properties and molecular forces of actomyosin extracted from two classes of chicken breast meat qualities (normal and pale, soft and exudative [PSE]-like) during heating process to further improve the understanding of the variations of functional properties between normal and PSE-like chicken breast meat. METHODS: Actomyosin was extracted from normal and PSE-like chicken breast meat and the gel strength, water-holding capacity (WHC), protein loss, particle size and distribution, dynamic rheology and protein thermal stability were determined, then turbidity, active sulfhydryl group contents, hydrophobicity and molecular forces during thermal-induced gelling formation were comparatively studied. RESULTS: Sodium dodecyl sulphate-polyacrylamide gel electrophoresis showed that protein profiles of actomyosin extracted from normal and PSE-like meat were not significantly different (p>0.05). Compared with normal actomyosin, PSE-like actomyosin had lower gel strength, WHC, particle size, less protein content involved in thermal gelation forming (p<0.05), and reduced onset temperature (To), thermal transition temperature (Td), storage modulus (G') and loss modulus (G″). The turbidity, reactive sulfhydryl group of PSE-like actomyosin were higher when heated from 40°C to 60°C. Further heating to 80°C had lower transition from reactive sulfhydryl group into a disulfide bond and surface hydrophobicity. Molecular forces showed that hydrophobic interaction was the main force for heat-induced gel formation while both ionic and hydrogen bonds were different significantly between normal and PSE-like actomyosin (p<0.05). CONCLUSION: These changes in chemical groups and inter-molecular bonds affected protein-protein interaction and protein-water interaction and contributed to the inferior thermal gelation properties of PSE-like meat.

ANXA1sp attenuates sepsis-induced myocardial injury by promoting mitochondrial biosynthesis and inhibiting oxidative stress and autophagy via SIRT3 upregulation.

Sepsis-induced myocardial injury is one of the most difficult complications of sepsis in intensive care units. Annexin A1 (ANXA1) short peptide (ANXA1sp) protects organs during the perioperative period. However, the protective effect of ANXA1sp against sepsis-induced myocardial injury remains unclear. We aimed to explore the protective effects and mechanisms of ANXA1sp against sepsis-induced myocardial injury both in vitro and in vivo. Cellular and animal models of myocardial injury in sepsis were established with lipopolysaccharide. The cardiac function of mice was assessed by high-frequency echocardiography. Elisa assay detected changes in inflammatory mediators and markers of myocardial injury. Western blotting detected autophagy and mitochondrial biosynthesis-related proteins. Autophagic flux changes were observed by confocal microscopy, and autophagosomes were evaluated by TEM. ATP, SOD, ROS, and MDA levels were also detected.ANXA1sp pretreatment enhanced the 7-day survival rate, improved cardiac function, and reduced TNF-α, IL-6, IL-1ß, CK-MB, cTnI, and LDH levels. ANXA1sp significantly increased the expression of sirtuin-3 (SIRT3), mitochondrial biosynthesis-related proteins peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α), and mitochondrial transcription factor A (TFAM). ANXA1sp increased mitochondrial membrane potential (△Ψm), ATP, and SOD, and decreased ROS, autophagy flux, the production of autophagosomes per unit area, and MDA levels. The protective effect of ANXA1sp decreased significantly after SIRT3 silencing in vitro and in vivo, indicating that the key factor in ANXA1sp's protective role is the upregulation of SIRT3. In summary, ANXA1sp attenuated sepsis-induced myocardial injury by upregulating SIRT3 to promote mitochondrial biosynthesis and inhibit oxidative stress and autophagy.

Comparative study of different dosages of grain-sized moxibustion on uterine artery blood flow in patients with cold and dampness primary dysmenorrhea. / ä¸åŒå‰‚é‡éº¦ç²’ç¸å¯¹å¯’æ¹¿å‡æ»žåž‹åŽŸå‘æ€§ç—›ç»æ‚£è€ å­å®«åŠ¨è„‰è¡€æµå½±å“çš„æ¯”è¾ƒç ”ç©¶.

OBJECTIVES: To observe the differences in the effects of different dosages of grain-sized moxibustion on uterine artery blood flow in patients with cold and dampness primary dysmenorrhea (PD). METHODS: A total of 60 patients with PD were randomly divided into 3 groups with 20 cases in each group. Acupoints Sanyinjiao (SP6), Diji (SP8) and Xuehai (SP10) were selected in all the 3 groups, and different dosages of grain-sized moxibustion were used (3 moxa cones, 6 moxa cones, 9 moxa cones) respectively. Treatment started 7 days before menstruation for 3 times, lasting for a total of 3 menstrual cycles. The values of uterine artery blood flow parameters including pulsatility index (PI), resistance index (RI), and systolic/diastolic ratio (S/D) were recorded before and after treatment. The visual analog scale (VAS) score and cox menstrual symptom scale (CMSS) score (including severity ［CMSS-S］ and time of duration ［CMSS-T］) were evaluated before treatment, at the end of each menstrual cycle, and one menstrual cycle after treatment. RESULTS: The values of uterine artery blood flow parameters (PI, RI, S/D) after treatment in the 9 moxa cones group were lower than those before treatment, as well as lower than those in the 3 and 6 moxa cones groups after treatment (P<0.05). The VAS scores of the 3 moxa cones group were lower than those before treatment in the first and second cycle (P<0.05). The VAS scores of the 6 and 9 moxa cones groups were lower than those before treatment at each observation point (P<0.05), and were lower than those of the 3 moxa cones group in the third cycle of treatment and follow-up period (P<0.05). And the VAS score of the 9 moxa cones group was lower than that of the 6 moxa cones group during the follow-up period (P<0.05). Compared with the scores before treatment, the CMSS-T scores at each observation point after treatment were lower in the 9 moxa cones group (P<0.05)；the CMSS-T scores in the second and third cycle after treatment, and follow-up period were lower in the 6 moxa cones group (P<0.05), with the CMSS-S scores in the second and third cycle after treatment, and follow-up period lower in the 6 and 9 moxa cones groups (P<0.05). The CMSS-T and CMSS-S scores of the 6 and 9 moxa cones groups were lower than those of the 3 moxa cones group in the third cycle and follow-up period (P<0.05). The CMSS-T and CMSS-S scores of the 9 moxa cones group were lower than those of the 6 moxa cones group during the follow-up period (P<0.05). CONCLUSIONS: Grain-Sized moxibustion has dose-effect relationship in the treatment of PD. Compared with 3 and 6 moxa cones groups, 9 moxa cones group has advantages in improving uterine artery blood flow parameters and alleviating dysmenorrhea symptoms in PD patients.

ROS-mediated MAPK activation aggravates hyperoxia-induced acute lung injury by promoting apoptosis of type II alveolar epithelial cells via the STAT3/miR-21-5p axis.

Inhibition of type II alveolar epithelial (AE-II) cell apoptosis is a critical way to cure hyperoxia-induced acute lung injury (HALI). It has been reported that miR-21-5p could reduce H2O2-induced apoptosis in AE-II cells. However, the upstream molecular mechanism remains unclear. Herein, we established a cellular model of HALI by exposing AE-II cells to H2O2 treatment. It was shown that miR-21-5p alleviated H2O2-induced apoptosis in AE-II cells. ROS inhibition decreased apoptosis of H2O2-evoked AE-II cells via increasing miR-21-5p expression. In addition, ROS induced MAPK and STAT3 phosphorylation in H2O2-treated AE-II cells. MAPK inactivation reduces H2O2-triggered AE-II cell apoptosis. MAPK activation inhibits miR-21-5p expression by promoting STAT3 phosphorylation in H2O2-challenged AE-II cells. Furthermore, STAT3 activation eliminated MAPK deactivation-mediated inhibition on the apoptosis of AE-II cells under H2O2 condition. In conclusion, ROS-mediated MAPK activation promoted H2O2-triggered AE-II cell apoptosis by inhibiting miR-21-5p expression via STAT3 phosphorylation, providing novel targets for HALI treatment.