PMID: 

Eur J Dermatol. 2002 Sep-Oct;12(5):422-7. PMID: 12370127

Abstract Title: 

Neuropeptides and sebaceous glands.

Abstract: 

This review provides a new insight into the participation of neuropeptides, notably substance P (SP), in the pathophysiology of acne. We show morphological alterations of sebaceous glands elicited by SP and differences in expression of various neurogenic factors in association with sebaceous glands in acne-prone versus normal facial skin. In vitro studies reveal that SP promotes both the proliferation and the differentiation of sebaceous glands. SP induces the expression of neutral endopeptidase, a potent neuropeptide-degrading enzyme, in sebaceous germinative cells and of E-selectin by perisebaceous venules. Facial skin from acne patients is characterized by rich innervation, by increased numbers of SP-containing nerves and mast cells, and by strong expression of neutral endopeptidase in sebaceous glands and E-selectin in venules around sebaceous glands, compared with normal skin. Mast cell-derived IL-6 and TNF-alpha, followed by SP-stimulated degranulation, have the potential to induce nerve growth factor expression by sebaceous cells which results in the promotion of innervation and in the expression of E-selectin, respectively. SP enhances mast cell proliferation through up-regulation of stem cell factor expression in fibroblasts. These findings suggest the involvement of neurogenic factors, such as neuropeptides, in the disease process of acne and explain the possible mechanism of the exacerbation of acne from a neurological point of view.

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PMID: 

Br J Dermatol. 2005 Nov ;153(5):919-24. PMID: 16225600

Abstract Title: 

Does facial sebum excretion really affect the development of acne?

Abstract: 

BACKGROUND: It is generally accepted that the severity of acne is correlated with facial sebum secretion. However, previous studies on the relation between seborrhoea and the development of acne did not consider topographical differences in facial sebum secretion and used relatively vague acne severity grading systems.OBJECTIVES: To elucidate the relation between topographical variations in facial sebum secretion and the severity of acne in women.METHODS: Forty-six female controls and 46 women with acne were included in this study. The Sebumeter was used to measure facial sebum secretion in the following facial areas: forehead, nose, chin, and right and left cheek. We counted noninflammatory comedones and inflammatory acne lesions in the same areas. We compared sebum secretion between patients with acne and controls, and analysed the relation between the quantity of sebum secreted and the number of acne lesions.RESULTS: Sebum secretions in the whole face and in the T- and U-zones (areas of high and low sebum secretion, respectively) were higher in patients with acne than in controls. There was no correlation between sebum quantity and acne lesion count in most facial regions.CONCLUSIONS: Increased levels of facial sebum secretion were observed in patients with acne. Our findings indicate that increased sebum levels do not directly cause development of acne lesions.

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PMID: 

Lipids Health Dis. 2010 Dec 9 ;9:141. Epub 2010 Dec 9. PMID: 21143923

Abstract Title: 

Clinical implications of lipid peroxidation in acne vulgaris: old wine in new bottles.

Abstract: 

Acne vulgaris is a common dermatological disorder, one that is frequently associated with depression, anxiety and other psychological sequelae. In recent years there has been an increasing focus on the extent to which oxidative stress is involved in the pathophysiology of acne. Emerging studies have shown that patients with acne are under increased cutaneous and systemic oxidative stress. Indeed, there are indications that lipid peroxidation itself is a match that lights an inflammatory cascade in acne. The notion that lipid peroxidation is a 'starter gun' in acne is not a new one; here we review the nearly 50-year-old lipid peroxidation theory and provide a historical perspective to the contemporary investigations and clinical implications.In addition, we present a novel hypothesis in which lipid peroxidation may be priming an increased susceptibility to co-morbid depression and anxiety in those with acne. The emerging research on the systemic burden of oxidative stress in acne sheds further light on the brain-skin axis. The recent findings also suggest potential avenues of approach for the treatment of acne via specific nutrients, dietary modifications, oral and topical interventions.

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PMID: 

Metabolites. 2019 Jun 11 ;9(6). Epub 2019 Jun 11. PMID: 31212603

Abstract Title: 

Cerebral Vitamin B5 (D-Pantothenic Acid) Deficiency as a Potential Cause of Metabolic Perturbation and Neurodegeneration in Huntington's Disease.

Abstract: 

Huntington's disease (HD) is a neurodegenerative disorder caused by an expanded CAG repeat in exon 1 of thegene. HD usually manifests in mid-life with loss of GABAergic projection neurons from the striatum accompanied by progressive atrophy of the putamen followed by other brain regions, but linkages between the genetics and neurodegeneration are not understood. We measured metabolic perturbations in HD-human brain in a case-control study, identifying pervasive lowering of vitamin B5, the obligatory precursor of coenzyme A (CoA) that is essential for normal intermediary metabolism. Cerebral pantothenate deficiency is a newly-identified metabolic defect in human HD that could potentially: (i) impair neuronal CoA biosynthesis; (ii) stimulate polyol-pathway activity; (iii) impair glycolysis and tricarboxylic acid cycle activity; and (iv) modify brain-urea metabolism. Pantothenate deficiency could lead to neurodegeneration/dementia in HD that might be preventable by treatment with vitamin B5.

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PMID: 

Am J Transl Res. 2019 ;11(8):5008-5018. Epub 2019 Aug 15. PMID: 31497217

Abstract Title: 

Vitamin B5 inhibit RANKL induced osteoclastogenesis and ovariectomy induced osteoporosis by scavenging ROS generation.

Abstract: 

B vitamins are a class of water-soluble vitamins that play important roles in cell metabolism. The participation of B vitamins in bone health has been recognized for decades. Pantothenic acid (vitamin B5) is mainly known for its wide variety of sources. However, the potential role of pantothenic acid in bone health and metabolism is still unclear. In this study, we found pantothenic acid has a dual effect on RANKL-induced osteoclastogenesis. Tartrate-resistant acid phosphatase (TRAP) stain shows that osteoclastogenesis was remarkably induced in a lower dosage of pantothenic acid (500 mM). We further confirmed this dual effect of pantothenic acid in osteoclastogenesis by detecting osteoclast formation and bone resorption using focal adhesion stain and pit formation, respectively. Mechanistically, we found phosphatidylinositol 3 kinase-protein kinase B (PI3K-Akt) pathway was activated in pre-osteoclasts (pOCs) after cultured with lower dosage of pantothenic acid; while the ROS generation was eliminated with upregulation of forkhead box O1 (FoxO1), forkhead box O2 (FoxO2) and NF-E2-related factor 2 (Nrf2) in pOCs after cultured with higher dosage of pantothenic acid. Finally, we used ovariectomized (OVX) mice to explore the potential role of pantothenic acid rich dietary in regulating bone metabolism, the result shows that pantothenic acid rich dietary can protect bone loss from estrogen deficiency. In brief, our study identified a new understanding of pantothenic acid in regulating osteoclastogenesis, revealed a therapeutic potential of pantothenic acid in prevention of bone loss related disorders.

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PMID: 

Ecotoxicol Environ Saf. 2019 Dec 15 ;185:109686. Epub 2019 Sep 20. PMID: 31546205

Abstract Title: 

Gestational B-vitamin supplementation alleviates PM-induced autism-like behavior and hippocampal neurodevelopmental impairment in mice offspring.

Abstract: 

Gestational exposure to PMis a worldwide environmental issue associated with long-lasting behavior abnormalities and neurodevelopmental impairments in the hippocampus of offspring. PMmay induce hippocampus injury and lead to autism-like behavior such as social communication deficits and stereotyped repetitive behavior in children through neuroinflammation and neurodegeneration. Here, we investigated the preventive effect of B-vitamin on PM-induced deleterious effects by focusing on anti-inflammation, antioxidant, synaptic remodeling and neurodevelopment. Pregnant mice were randomly divided into three groups including control group (mice subject to PBS only), model group (mice subject to both 30 μL PMof 3.456 μg/μL and 10 mL/(kg·d) PBS), and intervention group (mice subject to both 30 μL PMof 3.456 μg/μL and 10 mL/(kg·d) B-vitamin supplementation (folic acid, vitamin B6 and vitamin B12 with concentrations at 0.06, 1.14 and 0.02 mg/mL, respectively)). In the current study B-vitamin significantly alleviated neurobehavioral impairment reflected in reduced social communication disorders, stereotyped repetitive behavior, along with learning and spatial memory impairment in PM-stimulated mice offspring. Next, B-vitamin corrected synaptic loss and reduced mitochondrial damage in hippocampus of mice offspring, demonstrated by normalized synapse quantity, synaptic cleft, postsynaptic density (PSD) thickness and length of synaptic active area. Furthermore, significantly down-regulated expression of pro-inflammatory cytokines including NF-κB, TNF-α and IL-1β, and lipid peroxidation were found. We observed elevated levels of oxidant-related genes (SOD, GSH and GSH-Px). Moreover, decreased cleaved caspase-3 and TUNEL-positive cells suggested inhibited PM-induced apoptosis by B-vitamin. Furthermore, B-vitamin increased neurogenesis by increasing EdU-positive cells in the subgranular zone (SGZ) of offspring. Collectively, our results suggest that B-vitamin supplementation exerts preventive effect on autism-like behavior and neurodevelopmental impairment in hippocampus of mice offspring gestationally exposed to PM, to which alleviated mitochondrial damage, increased anti-inflammatory and antioxidant capacity and synaptic efficiency, reduced neuronal apoptosis and improved hippocampal neurogenesis may contribute.

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PMID: 

Diabetol Metab Syndr. 2019 ;11:86. Epub 2019 Oct 26. PMID: 31673295

Abstract Title: 

Effects of vitamin D supplementation on advanced glycation end products signaling pathway in T2DM patients: a randomized, placebo-controlled, double blind clinical trial.

Abstract: 

Background: Several researches have recommended vitamin D possible health benefits on diabetic complications development, but a few number of studies have been accomplished on the molecular and cellular mechanisms. Certain cellular pathways modification and also some transcription factors activation may protect cells from hyperglycemia condition induced damages. This study purpose was to determine the vitamin D supplementation effect on some key factors [advanced glycation end products (AGEs) signaling pathway] that were involved in the diabetic complications occurrence and progression for type-2 diabetes participants.Methodology: 48 type-2 diabetic patients (T2DM) randomly divided into two groups (n = 24 per group), receiving: 100-µg vitamin D or placebo for 3 months. At this study beginning and the end, the receptor expression for advanced glycation end products (RAGE) and glyoxalase I (GLO1) enzyme from peripheral blood mononuclear cells (PBMCs) and AGEs and tumor necrosis factor-α (TNF-α) serum levels were measured by the use of real-time PCR and ELISA methods, respectively.Results: This study results demonstrated that vitamin D supplementation could down-regulate RAGE mRNA [fold change = 0.72 in vitamin D vs. 0.95 in placebo) P = 0.001)]. In addition, no significant changes were observed for GLO1 enzyme expression (P = 0.06). This study results also indicated that vitamin D serum level significantly increased in vitamin D group (P 

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PMID: 

Horm Metab Res. 2019 Nov ;51(11):729-734. Epub 2019 Nov 4. PMID: 31683343

Abstract Title: 

Could Vitamin D be Associated with Proliferative Diabetic Retinopathy? Evidence from Pooling Studies.

Abstract: 

Contrasting data about the association between proliferative diabetic retinopathy (PDR) and vitamin D status remain unknown. First, a hospital-based cross-sectional study consisting of 889 diabetic retinopathy (DR) and non-DR (NDR) patients was admitted. Further the accumulated evidence was performed to explore the association and dose-response relationship. Our study indicated that the odd ratio for PDR in vitamin D deficiency (VDD) individuals was significantly increased (1.60, 95% CI 1.06-2.42), compared with NDR in vitamin D sufficiency individuals, adjusted by age, sex, diabetic duration, and HbA1c. Four studies plus our study with data on vitamin D levels in 4970 patients with PDR and NDR subjects are compared. Association between vitamin D deficiency and risk of PDR exists (OR=1.69, 95% CI 1.40-2.05; I=0%, p=0.61). Association between a nonlinear trend for vitamin D decrease with risk of DR was significant (chi=16.53, p=0.0003). No significant heterogeneity in identified studies was found (goodness of fit chi=2.98, p=0.225). It is concluded that vitamin D deficiency is significantly associated with risk of proliferative diabetic retinopathy.

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PMID: 

Nutr Metab (Lond). 2019 ;16:34. Epub 2019 May 22. PMID: 31139236

Abstract Title: 

Whole blueberry protects pancreatic beta-cells in diet-induced obese mouse.

Abstract: 

Background: Blueberry is rich in bioactive substances and possesses powerful antioxidant potential, which can protect against oxidant-induced and inflammatory cell damage and cytotoxicity. The aim of this study was to determine how blueberry affects glucose metabolism and pancreaticβ-cell proliferation in high fat diet (HFD)-induced obese mice.Methods: Wild type male mice at age of 4 weeks received two different kinds of diets: high-fat diet (HFD) containing 60% fat or modified HFD supplemented with 4% (wt:wt) freeze-dried whole blueberry powder (HFD + B) for 14 weeks. A separate experiment was performed in mice fed with low-fat diet (LFD) containing 10% fat or modifiedLFD + B supplemented with 4% (wt:wt) freeze-dried whole blueberry powder. The metabolic parameters including blood glucose and insulin levels, glucose and insulin tolerances were measured.Results: Blueberry-supplemented diet significantly increased insulin sensitivity and glucose tolerance in HFD + B mice compared to HFD mice. However, no difference was observed in blood glucose and insulin sensitivity between LFD + B and LFD mice. In addition, blueberry increased β-cell survival and prevented HFD-induced β-cell expansion. The most important finding was the observation of presenceof small scattered islets in blueberry treated obese mice, which may reflect a potential role of blueberry in regenerating pancreatic β-cells.Conclusions: Blueberry-supplemented diet can prevent obesity-induced insulin resistance by improving insulin sensitivity and protecting pancreaticβ-cells. Blueberry supplementation has the potential to protect and improve health conditions for both type 1 and type 2 diabetes patients.

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PMID: 

Biomed Rep. 2019 Nov ;11(5):207-214. Epub 2019 Sep 10. PMID: 31632668

Abstract Title: 

Protective functions of Lycium barbarum polysaccharides in HO-injured vascular endothelial cells through anti-oxidation and anti-apoptosis effects.

Abstract: 

Cell injury in the cardiovascular endothelia caused by oxidative stress is among the major inducers of endothelium dysfunction and serves an important role in initiating cardiovascular diseases (CVDs). Therefore, protecting and improving the normal function of endothelial cells are considered key measures against CVDs. As a traditional Chinese medicinal component,is regarded to have high medicinal value. The present study aimed to investigate the potential anti-apoptosis and anti-oxidation effects ofpolysaccharides (LBPs) on injured rat artery endothelial cells, to demonstrate the experimental and medicinal values of LBPs. In the present study, the aortic endothelial cells of rats were cultivated and randomly divided into five groups: A control group, HO-injured group (HOgroup), HO+LBPs (110µg/ml) group (low-dose group, LT), HO+LBPs (220µg/ml) group (medium-dose group, MT) and HO+LBPs (440µg/ml) group (high-dose group, HT). Among these, the activity of superoxide dismutase (SOD), and the levels of malondialdehyde (MDA) and nitric oxide (NO) were detected by colorimetry. Additionally, the expression of B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax) were detected by western blotting. It was observed that SOD activity and NO content decreased while MDA content increased significantly in the HOgroup (P

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