Effects of oat ß-glucan on the retrogradation behavior of rice starch and its potential mechanism.

In this study, to minimize the quality deterioration caused by the retrogradation of starch-based food, the effect and mechanism of oat ß-glucan (OG) on the retrogradation of rice starch was investigated. OG effectively decreased storage modulus (G'), syneresis, and retrogradation enthalpy, indicating the inhibition of short-term and long-term retrogradation of rice starch. The competition for water molecules between the OG and rice starch resulted in partial swelling of the starch granules, consequently reducing particle size, lowering amylose leaching, and decreasing the proportion of short-amylose chains. The microstructure characterization showed that the OG-treated rice starch group (ST-OG) exhibited a smoother and denser surface. Particularly, no notable alterations were observed in the structure of the ST-OG sample during storage, owing to the improved water-holding capacity of starch gel and reduced proportion of free water caused by OG. Furthermore, the ordered structure results confirmed the occurrence of hydrogen bonding between OG and rice starch, which hindered the rearrangement of starch molecules. Therefore, OG is an effective natural additive for controlling the retrogradation of starch-based foods.

Aquaporin 7 is upregulated through the PI3K-Akt pathway and modulates decidualisation of endometrial stromal cells.

CONTEXT: Aquaporin 7 (AQP7) is selectively expressed in decidualised endometrial stromal cells (ESCs) of mice surrounding the embryonic implantation sites. However, the roles of AQP7 and the underlying mechanism that regulates AQP7 expression in endometrial decidualisation after implantation are still unclear. AIMS: This study aimed to investigate the role of the PI3K-Akt pathway in regulating the expression of AQP7 in ESCs and decidualisation. METHODS: Primary ESCs of pregnant mice were isolated to establish in vitro decidualisation models. PI3K inhibitor LY294002 was added to the decidualisation models, then AQP7 expression, changes in decidualised ESC morphology and expression of decidualisation marker molecules were examined. KEY RESULTS: AQP7 knockdown reduced the proliferation and differentiation of ESCs with in vitro induced decidualisation. Furthermore, when the activity of PI3K was inhibited by LY294002, the expression of AQP7 in decidualised ESCs was decreased and both the proliferation and differentiation of ESCs were significantly reduced. CONCLUSIONS: This indicates that AQP7 is a key molecule involved in endometrial decidualisation and the expression of AQP7 is upregulated through activation of the PI3K-Akt pathways, which promotes the proliferation and differentiation of the ESCs, thus affecting occurrence of decidualisation. IMPLICATIONS: This study may provide a new biomarker for the diagnosis of infertility and a new drug target for the prevention and treatment of infertility.

Purple sweet potato color attenuates high fat-induced neuroinflammation in mouse brain by inhibiting MAPK and NF-κB activation.

Purple sweet potato color (PSPC) is a natural anthocyanin pigment that is derived from purple sweet potato storage roots. PSPC possesses a variety of biological activities, including antioxidant, anti­inflammatory and neuroprotective effects; however, the detailed effects of PSPC on high­fat diet (HFD)­induced neuroinflammation remain to be determined. The aim of the present study was to investigate whether PSPC has a protective role in HFD­associated neuroinflammation in the mouse brain and to provide novel insight into the mechanisms of the action. C57BL 6J mice were maintained on a normal diet (10 kcal% fat), a HFD (60 kcal% fat), a HFD with PSPC (700 mg/kg/day) or PSPC alone, which was administrated over 20 weeks. Open field and step­through tests were used to evaluate the effects of HFD and PSPC on mouse behavior and memory function. Western blotting and ELISA analyses were used to assess the expression of inflammatory cytokines and the activation of mitogen­activated protein kinase and nuclear factor­κB (NF­κB). The results demonstrated that PSPC treatment was able to significantly improve the HFD­induced impairment of mouse behavior and memory function, and suppressed the increase in body weight, fat content, hyperlipemia and the level of endotoxin. PSPC treatment also markedly decreased the expression of cyclooxygenase­2, inducible nitric oxide synthase, tumor necrosis factor­α, interleukin (IL)­1ß and IL­6, and increased the level of IL­10 in the HFD­treated mouse brain. In addition, PSPC inhibited the HFD­induced phosphorylation of extracellular signal­regulated kinase (ERK), c­Jun N­terminal kinase (JNK) and p38, and the activation of NF­κB. These findings indicated that PSPC treatment may alleviate HFD­induced neuroinflammation in the mouse brain by inhibiting ERK, JNK, p38 and NF-κB activation.

Spata19 is critical for sperm mitochondrial function and male fertility.

Haploid round spermatids undergo differentiation and morphogenesis during spermiogenesis, resulting in mature spermatozoa. The molecular details underlying this transformation, however, remain poorly understood. In this study, we generated and analyzed germ cell-specific Spata19 knockout mice (Spata19(flox/flox) ; Stra8-Cre; hereafter termed "Spata19 cKO") to assess the model that SPATA19 contributes to mitochondrial function in differentiating spermatids. Spata19-cKO males were infertile, as their sperm exhibited disorganized mitochondrial structure; furthermore, their sperm-abundance of mitochondrial proteins, activities of mitochondrial respiratory chain complex IV, and ATP levels were significantly reduced. Yet, the infertility of Spata19-cKO males was rescued by intracytoplasmic sperm injection, so the sperm are capable of initiating development. Collectively, our findings suggest that SPATA19 plays an important role in sperm motility by regulating the organization and function of the mitochondria.

Voltage-dependent anion channels (VDACs) promote mitophagy to protect neuron from death in an early brain injury following a subarachnoid hemorrhage in rats.

The term mitophagy is coined to describe the selective removal of mitochondria by autophagy but the process itself is still contentious, especially in the early period following subarachnoid hemorrhage (SAH). In the present study, we investigated the role of mitophagy following 48h after SAH injury in rats. Specifically evaluating whether mitophagy, through voltage dependant anion channels (VDACs) interacting with microtubule-associated protein 1 light chain 3, could orchestrate the induction of apoptotic and necrotic cell death in neurons, a VDAC1siRNA and an activitor Rapamycian (RAPA), were engaged. One hundred and twelve male Sprague-Dawley rats were randomly divided into 4 groups: Sham, SAH, SAH+VDAC1siRNA, and SAH+RAPA. Outcomes measured included mortality rate, brain edema, BBB disruption, and neurobehavioral testing. We also used western blotting techniques to analyze the expressions of key mitophagic/autophagic proteins and pro-apoptotic protein such as ROS, VDAC1, LC-3II and Caspase-3. Rapamycin treatment significantly improved the mortality rate, cerebral edema, and neurobehavioral deficits; apoptotic and necrotic cell death in neurons were reduced by Rapamycin following SAH injury. However, VDAC1siRNA worsened the brain injury following SAH. Immunohistochemical staining and western blot analysis demonstrated a decreased expression of VDAC1, LC3II, and an increase of ROS and Caspase-3 followed by VDAC1siRNA administration. In conclusion, mitophagy induced by VDAC1 following SAH injury may in fact play a significant role in neuroprotection, the mechanism which may be through the attenuation of the apoptosic and necrosic molecular pathways. This translates a preservation of functional integrity and an improvement in mortality.