Roles of Ferulic acid on muscle atrophy and grip strength in diabetic mice.

Diabetes is an inducement of muscle atrophy to cause motor disturbance. Ferulic Acid (FA) possessed various pharmacological effects in diabetes and muscle function. This research aimed to appraise potential role of FA on muscle atrophy in high glucose environment. Our result displayed FA promoted myofiber size and grip strength to reduce high glucose-mediated muscle function discords. In serum, FA exhibited its anti-oxidative and anti-inflammatory capabilities via enhancing T-AOC, SOD and CAT levels and reducing MDA, TNF-α and IL-6 levels. In skeletal muscle, FA suppressed FBXO-32 and MURF-1 expressions to improve ubiquitin-proteasome system. Moreover, GA restrained DDIT-3 and GRP-78 expressions to relieve high glucose-mediated endoplasmic reticulum stress. Lastly, GA increased BAX expressions and decreased BCL-2 expressions to attenuate high glucose-mediated apoptosis. In conclusion, FA preserve against muscle atrophy by meliorating ubiquitin-proteasome system, endoplasmic reticulum stress and apoptosis in high glucose environment.

Asiatic acid ameliorates life and health span in fruit fly.

Aging is becoming a prominent health problem in present world. Asiatic acid has multiple health-protecting effects because of its variety biological function. However, relation between asiatic acid and aging is still unknown. In this study, fruit fly was used as model animal to illuminate anti-aging effect of asiatic acid. Our results advised asiatic acid possessed efficacy of promoting health span, as represented by extending lifetime and enhancing locomotor activity both in intrinsic and pathologically aging. In external environment, asiatic acid elevated survival rate against oxidative response and starvation resistance. In aspect of anti-aging mechanism, asiatic acid possessed antioxidant capacity by improvement of super oxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-px) activities and suppression of malondialdehyde (MDA) level to promote health span. In addition, asiatic acid amended energy material storage to meet needs of life process. Moreover, asiatic acid inhibited acetylcholine (AChE) activity to alter cholinergic system in aging process. Lastly, asiatic acid upregulated peroxisome proliferator-activated receptor gamma coactivator 1 (PGC1) and silence information regulator 2 (Sir2) expression in intrinsic aging. In conclusion, asiatic acid exerted health-protecting potential via modulating directly or indirectly antioxidant activity, cholinergic system and longevity genes and could be developed into anti-aging agent.

Overexpression of Nmnat improves the adaption of health span in aging Drosophila.

Nmnat is a stress response protein which has been involved in a variety of biological processes. However, the effects of Nmnat on aging have not yet been investigated. The present study revealed the effects of Nmnat on aging of Drosophila and uncovered its underlying mechanism. Therefore, the overexpression of Nmnat was established by arm/Gal4 system in Drosophila with an aim to determine the functions of Nmnat during aging process. In this study, our results showed Nmnat was a positive factor on lifespan and movement capacity, which was consistent on d-galactose induced aging acceleration. Further investigation showed that oxidative stress biomarkers, longevity gene, mitochondria related genes and ATP levels were significantly improved in the Nmnat overexpression Drosophila, which suggested that the underlying mechanism of Nmnat on aging process and movement capacity was partly due to its anti-oxidative stress and mitochondrial-protection function. In addition, on H2O2 challenge tests, Nmnat overexpression was sufficient to increase the survival time and movement capacity of Drosophila, which was probably due to its protection against oxidative stress. On rotenone induced mitochondrial dysfunction, Nmnat overexpression also showed better health span and movement capacity than the control group. Based on these data, Nmnat may be a new molecular target to improve health span by enhancing stress resistance and locomotor activity in aging process.

WITHDRAWN: Regular exercise protects aging Drosophila from high-fat-diet-induced locomotor impairment, cardiac dysfunction, lifespan shortening, and Nmnat and dSir2 expression decline.

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Anatomic study of the position of the mandibular canal and corresponding mandibular third molar on cone-beam computed tomography images.

PURPOSE: The positional relationship between the mandibular canal and corresponding third molars is a key anatomic factor of inferior alveolar nerve (IAN) injury. The aim of the present study is to classify the anatomic three-dimensional relationship between the mandibular third molar and the mandibular canal on cone-beam computed tomography (CBCT) images. METHODS: This study used CBCT images to classify the positional relationship between the mandibular canal and corresponding third molars. CBCT images of 749 patients (1296 mandibular third molars) were analyzed to draw up a classification. RESULTS: On a total of 1296 third molars, the mandibular canal relative to the roots of the mandibular third molar was on the apical side (88.1%), followed by the buccal side (7.9%), the lingual side (3.5%), and then between the roots (0.5%). Ninety-five (7.1%) third molars had a close relation with the mandibular canal, while 1201 (92.7%) third molars had no direct contact. The percentage of the mandibular canal contacts with the mandibular third molar was higher when the mandibular canal was lingually positioned. CONCLUSIONS: The anatomic structures of the mandibular third molar and the mandibular canal may be helpful to make adequate surgical planning to avoid or reduce nerve involvement.

Comparison of digital panoramic radiography versus cone beam computerized tomography for measuring alveolar bone.

BACKGROUND: Cone beam computerized tomography (CBCT) has been widely used in dental implanting. However, the local hospitals usually don't have access to CBCT due to the cost and medical investment, especially in West of China. The doctors in local hospitals have to make reasonable dental planting using orthopantomography (OPG) to reduce risks. Therefore, it is clinically meaningful to determine the magnification rate of OPG to obtain correct diagnosis. This study investigated the magnification rate of OPG in measuring different maxillofacial loci compared with CBCT. METHODS: Eighty-six patients demanding dental implanting were scanned by CBCT and OPG. The vertical distance between the alveolar ridge crest of the maxillary first molar and the sinus bottom of the upper jaw, the distance between the alveolar ridge crest of the mandibular first molars and the top of nerviduct in the mandibular alveolar, and the distance between the alveolar ridge crest of the maxillary central incisors and the bottoms of the nasal cavities were measured. The horizontal distance in those loci were also measured. The distances derived from CBCT were used as reference. The distances between the two methods were compared using paired t-test. The magnification rates at these positions were calculated. The relationship between the data acquired from the two methods was analyzed Pearson correlation. RESULTS: The correlation coefficients (R) between the paired samples obtained from OPG and CBCT were highly related (P < 0.05) with R values varying from 0.840 and 0.959 in vertical distances and R values varying from 0.703 and 0.904 in horizontal distances. Compared with data obtained from CBCT, the mean vertical magnification rates were 11.38% and 12.95% vertically and 8.55% and 9.43% horizontally for the first molars in the right and left maxilla respectively; 7.26% and 6.35% vertically and 5.33% and 4.96% horizontally for the first molars in the right and left mandible respectively; and 5.55% and 4.84% vertically and 6.53% and 7.47% horizontally for the central incisors in the upper right and left jaws respectively. CONCLUSION: The magnification rates of OPG at these teeth are different. The distances measured by OPG were highly correlated with that measured by CBCT.

Naringin ameliorates cognitive deficits in streptozotocin-induced diabetic rats.

OBJECTIVES: Previous research demonstrated that diabetes is one of the leading causes of learning and memory deficits. Naringin, a bioflavonoid isolated from grapefruits and oranges, has potent protective effects on streptozotocin (STZ)-induced diabetic rats. Recently, the effects of naringin on learning and memory performances were monitored in many animal models of cognitive impairment. However, to date, no studies have investigated the ameliorative effects of naringin on diabetes-associated cognitive decline (DACD). In this study, we investigated the effects of naringin, using a STZ-injected rat model and explored its potential mechanism. MATERIALS AND METHODS: Diabetic rats were treated with naringin (100 mg/kg/d) for 7 days. The learning and memory function were assessed by Morris water maze test. The oxidative stress indicators [superoxide dismutase (SOD) and malondialdehyde (MDA)] and inflammatory cytokines (TNF-a, IL-1ß, and IL-6) were measured in hippocampus using corresponding commercial kits. The mRNA and protein levels of PPARγ were evaluated by real time (RT)-PCR and Western blot analysis. RESULTS: The results showed that supplementation of naringin improved learning and memory performances compared with the STZ group. Moreover, naringin supplement dramatically increased SOD levels, reduced MDA levels, and alleviated TNF-α, IL-1ß, and IL-6 compared with the STZ group in the hippocampus. The pretreatment with naringin also significantly increased PPARγ expression. CONCLUSION: Our results showed that naringin may be a promising therapeutic agent for improving cognitive decline in DACD.

CXXC5 is required for cardiac looping relating to TGFß signaling pathway in zebrafish.

BACKGROUND: CXXC-type zinc-finger protein CXXC5 has been reported to be associated with the development of cardiovascular disease. Recently, through signaling pathway screening we found that CXXC5 activated Tgfß and myocardial differentiation signaling pathways simultaneously. Although the physiological and pathological function of CXXC5 in many organs has been well elucidated, its function in heart remains unclear. METHODS AND RESULTS: Here, we found that zebrafish CXXC5 and SMAD were interacting through ZF-CXXC and MH1 domain. Over-expression of CXXC5 in cardiomyocyte increased the luciferase report activity of Tgfß signaling pathway. Spatiotemporal expression profile of cxxc5 showed that it consistently expressed during cardiogenesis. Knockdown of cxxc5 in zebrafish displayed looping defects, cardiac dysplasia, pericardial edema, and decreased contraction ability, accompanied with down-regulation of members referring to cardiac looping downstream genes of Tgfß signaling pathway, such as nkx2.5, hand2, and has2. Co-injection of hand2 mRNA with cxxc5 morpholino rescued the cardiac looping detects. CONCLUSION: Our study is the first to provide an in vivo evidence for cxxc5 regulating heart development and cardiac looping via Tgfß related signaling pathway. This finding suggested that CXXC5 may serve as a possible marker that has potential diagnostic and prognostic value in fetus with congenital heart disease.

Puerarin ameliorates cognitive deficits in streptozotocin-induced diabetic rats.

Previous research has indicated that Diabetes is a high risk of learning and memory deficits. Puerarin, an isoflavonoid extracted from Kudzu roots, has been reported to possess antioxidant, anti-inflammatory, anti-apoptotic and anti-diabetic properties which are useful in the treatment of various diseases. Recently, Puerarin was found to have the effects on learning and memory performances in humans and animal models. However, up to now, there is no detailed evidence on the effect of Puerarin on diabetes-associated cognitive decline (DACD). In this study, we designed to assess the effects of Puerarin on diabetes-associated cognitive decline (DACD) using a streptozotocin (STZ)-injected rat model and exploring its potential mechanism. Diabetic rats were treated with Puerarin (100 mg/kg per d) for 7 days. The learning and memory function was evaluated by morris water maze test. The acetylcholinesterase (AChE), choline acetylase (ChAT), oxidative indicators [malondialdehyde (MDA) and superoxide dismutase (SOD)] and inflammatory cytokine (TNF-a, IL-1ß and IL-6) were measured in hippocampus by using corresponding commercial kits. mRNA and Protein levels of Bcl-2 were analyzed by RT-PCR and Westernblot. The results showed that supplementation of Puerarin improved the learning and memory performances compared with the STZ group by the morris water maze test. In addition, Puerarin supplement significantly prevented AChE and MDA activities, increased ChAT and SOD activities, and alleviated the protein level of TNF-α, IL-1ß and IL-6 in the hippocampus compared with the STZ group. Moreover, the pretreatment with Puerarin also significantly increased the Bcl-2 expression. It is concluded that Puerarin possesses neuroprotection to ameliorate cognitive deficits in streptozotocin-induced diabetic rats by anti-inflammatory, antioxidant and antiapototic effects.

CXXC5 regulates differentiation of C2C12 myoblasts into myocytes.

CXXC5 is a member of the CXXC-type zinc-finger domain containing protein family, which is suggested to function in gene transcription, cell adhesion and cytoskeleton organization. Previous studies have revealed that CXXC5 is expressed in skeletal muscle, but whether it regulates skeletal myogenesis is yet unknown. Here, we screened for the possible signaling pathways in which CXXC5 might participate using luciferase gene reporters. The results indicated that CXXC5 significantly increased the activities of the promoters of genes involved in skeletal muscle differentiation. We therefore studied the role of CXXC5 during skeletal myogenesis in C2C12 myoblasts. Our findings suggest that overexpression of CXXC5 in C2C12 myoblasts facilitated myocyte differentiation, while RNAi interference of CXXC5 significantly inhibited the differentiation of C2C12 myoblasts. This study suggests that CXXC5 plays a significant role in regulating skeletal myogenesis.