Walnut protein hydrolysates, rich with peptide fragments of WSREEQEREE and ADIYTEEAGR ameliorate UV-induced photoaging through inhibition of the NF-κB/MMP-1 signaling pathway in female rats

2020 ◽  
Vol 11 (12) ◽  
pp. 10601-10616
Author(s):  
Defeng Xu ◽  
Weiqiong Wang ◽  
Jianmeng Liao ◽  
Lan Liao ◽  
Caihong Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Pathological Process ◽  
Protein Hydrolysates ◽  
Female Rats ◽  
Peptide Fragments ◽  
Skin Photoaging ◽  
Inflammatory Regulation

Skin photoaging is a complicated pathological process, and the imbalance of inflammatory regulation is associated highly with photoaging progression.

Attenuation of UV-induced skin photoaging in rats by walnut protein hydrolysates is linked to enhancement of antioxidant capacity, modulation of MAPK/AP-1/TGF-β/Samd signaling pathway, and promotion of type Ⅰ procollagen synthesis

2021 ◽  
Author(s):  
Defeng Xu ◽  
Caihong Li ◽  
Mouming Zhao
Keyword(s):  
Oxidative Stress ◽  
Oral Administration ◽  
Antioxidant Capacity ◽  
Signaling Pathway ◽  
Protein Hydrolysates ◽  
Skin Photoaging ◽  
Capacity Modulation

There is growing evidences that prevention of skin photoaging by oral administration of food-derived proteins hydrolysates is intricately linked to its alleviation against oxidative stress through modulation of signaling pathway....

scholarly journals Leptin and glucocorticoid signaling pathways in the hypothalamus of female and male fructose-fed rats

2014 ◽  
Vol 66 (2) ◽  
pp. 829-839 ◽  
Author(s):  
Danijela Vojnovic-Milutinovic ◽  
Marina Nikolic ◽  
Jovana Dinic ◽  
Ana Djordjevic ◽  
Natasa Velickovic ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Signaling Pathway ◽  
Leptin Receptor ◽  
Female Rats ◽  
Male Rats ◽  
Cytokine Signaling ◽  
Mrna Levels ◽  
Leptin Sensitivity ◽  
Male And Female Rats ◽  
Glucocorticoid Signaling

Alterations in leptin and glucocorticoid signaling pathways in the hypothalamus of male and female rats subjected to a fructose-enriched diet were studied. The level of expression of the key components of the leptin signaling pathway (neuropeptide Y /NPY/ and suppressor of cytokine signaling 3 /SOCS3/), and the glucocorticoid signaling pathway (glucocorticoid receptor /GR/, 11?-hydroxysteroid dehydrogenase type 1 /11?HSD1/ and hexose-6-phosphate dehydrogenase /H6PDH/) did not differ between fructose-fed rats and control animals of both genders. However, in females, a fructose-enriched diet provoked increases in the adiposity index, plasma leptin and triglyceride concentrations, and displayed a tendency to decrease the leptin receptor (ObRb) protein and mRNA levels. In male rats, the fructose diet caused elevations in plasma non-esterified fatty acids and triglycerides, as well as in both plasma and hypothalamic leptin concentrations. Our results suggest that a fructose-enriched diet can induce hyperleptinemia in both female and male rats, but with a more pronounced effect on hypothalamic leptin sensitivity in females, probably contributing to the observed development of visceral adiposity.

scholarly journals EXPERIMENTAL APPROVAL OF THE EFFICACY OF THE COMBINED COMPOSITION RECTAL CREAM NEW TEST-SAMPLES IN THE CONDITIONS OF ACUTE COMPLICATED ANAL FISSURE IN RATS

2019 ◽  
Vol 4 ◽  
pp. 42-49
Author(s):  
Ganna Zaychenko ◽  
Marina Stakhorska
Keyword(s):  
Anal Fissure ◽  
Muscle Tone ◽  
Inhibitory Effect ◽  
Pathological Process ◽  
Female Rats ◽  
Important Place ◽  
Modified Model ◽  
Local Bleeding ◽  
Severity Of The Disease

Anal fissure (AF) is one of the most common anorectal problems. The severity of the disease, the chronicity of the pathological process and frequent complications lead to a sharp deterioration in the quality of life of patients. An important place in the treatment of anal fissure is occupied by drugs that affect its key mechanism of pathogenesis, namely, reduce the muscle tone of the internal anal sphincter and have anti-inflammatory, analgesic, and reparative properties. Aim: conducting of screening studies of the effectiveness of new test samples of rectal cream of the combined composition (RCCC) on the model of acute complicated anal fissure in rats and determining the optimal composition of the potential drug. Materials and methods. The research was conducted on the basis of the Central Scientific Research Laboratory of the National Pharmaceutical University (CSRL NUPH) in the spring (April) season of 2015 on the female rats. A study of test specimens of the rectal cream of the combined composition was performed on a modified model of acute anal fissure. The effectiveness of the treatment was evaluated in terms of (0 to 2) severity of edema, hyperaemia, local bleeding, purulent necrotic processes, scapular formation, anatomical defect, and a general indicator of the severity of the pathological process (by the sum of the points for all the criteria that were analyzed). The level of proinflammatory PGE2 in serum was determined by the immune enzyme method. Results. The RCCC sample No. 4 showed the most expressive therapeutic effect among the four samples under study, and had credible benefits to the inhibitory effect on purulent-necrotic processes, as expressed by the differences in the overall rate of the pathological process (6 days: 5.83±0.47 points against 7.00±0.37; 7.83±0.31 under the influence of RCCC No. 2, No. 3, respectively, and for 11 days 5.00±1.03 versus 6.83±1.28 points (p=0.08 ) under the influence of RCCC No. 1). The ability of RCCCs No.1 and No.4 to reduce the level of pro-inflammatory PGE2 in blood serum of rats compared with CP in 1.8 and 2.0 times, respectively, contributed to accelerating epithelization and scar formation. The advantages of RCCC No. 4 on the comparison of the ointment "Proctozan" with the reduction of the period of epithelization of the defect of the mucous membrane of the anal canal for 3 days (for 7 days – RCCC No. 4, for 10 days - ointment "Proctozan"). Conclusions. The rectal cream of the combined composition No. 4 showed the greatest efficacy, had advantages over the comparison ointment "Proctozan", and is promising for the creation on its basis a new drug for the treatment of anal fissures.

scholarly journals Role of Nrf2 and Its Activators in Cardiocerebral Vascular Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-19
Author(s):  
Liangkai Cheng ◽  
Hong Zhang ◽  
Fang Wu ◽  
Zhongqiu Liu ◽  
Yuanyuan Cheng ◽  
...  
Keyword(s):  
Vascular Disease ◽  
Signaling Pathway ◽  
Redox Regulation ◽  
Antioxidant Response ◽  
Pathological Process ◽  
Cellular Damage ◽  
Common Disease ◽  
High Morbidity ◽  
Therapeutic Drugs

Cardiocerebral vascular disease (CCVD) is a common disease with high morbidity, disability, and mortality. Oxidative stress (OS) is closely related to the progression of CCVD. Abnormal redox regulation leads to OS and overproduction of reactive oxygen species (ROS), which can cause biomolecular and cellular damage. The Nrf2/antioxidant response element (ARE) signaling pathway is one of the most important defense systems against exogenous and endogenous OS injury, and Nrf2 is regarded as a vital pharmacological target. The complexity of the CCVD pathological process and the current difficulties in conducting clinical trials have hindered the development of therapeutic drugs. Furthermore, little is known about the role of the Nrf2/ARE signaling pathway in CCVD. Clarifying the role of the Nrf2/ARE signaling pathway in CCVD can provide new ideas for drug design. This review details the recent advancements in the regulation of the Nrf2/ARE system and its role and activators in common CCVD development.

Rice protein hydrolysates (RPHs) inhibit the LPS-stimulated inflammatory response and phagocytosis in RAW264.7 macrophages by regulating the NF-κB signaling pathway

RSC Advances ◽  
2016 ◽  
Vol 6 (75) ◽  
pp. 71295-71304 ◽  
Author(s):  
Li Wen ◽  
Yuehua Chen ◽  
Li Zhang ◽  
Huixin Yu ◽  
Zhou Xu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Protein Hydrolysates ◽  
Rice Protein ◽  
Phagocytic Ability ◽  
Raw264.7 Macrophages ◽  
Tnf Α

Different RPH components inhibit LPS-induced NO and TNF-α production. RPHs-C-7-3 inhibits the expression of pro-inflammatory expression. RPHs-C-7-3 suppresses the LPS-stimulated phagocytic ability. RPHs-C-7-3 regulates the nuclear translocation of p65.

scholarly journals Moxibustion Inhibits the ERK Signaling Pathway and Intestinal Fibrosis in Rats with Crohn’s Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Xiaomei Wang ◽  
Yuan Lu ◽  
Luyi Wu ◽  
Chen Zhao ◽  
Chunbin Song ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Signaling Pathway ◽  
Pathological Process ◽  
Erk Signaling ◽  
Control Group ◽  
Mrna Levels ◽  
Colon Tissue ◽  
Intestinal Fibrosis ◽  
Mild Moxibustion

Intestinal fibrosis is the main pathological process in Crohn’s disease (CD); acupuncture and moxibustion can inhibit the process of fibrosis in CD rats, but the regulatory mechanism remains unknown. The present study observed the effect of moxibustion on the extracellular signal-regulated kinase (ERK) signaling pathway in the CD rat. The result shows that the phosphorylation of the Ras, Raf-1, MEK-1, and ERK-1/2 proteins and the expression of the corresponding mRNAs in the colon tissue of CD rat were significantly higher than the normal control group. Both treatments with mild moxibustion and with herb-separated moxibustion significantly reduced the expression of the Ras, Raf-1, MEK-1, and ERK-1/2 proteins and Ras and Raf-1 mRNA. MEK-1 and ERK-1/2 mRNA expression in each treatment group showed a downward trend, and the ERK-1/2 mRNA levels were significantly lower in the mild moxibustion group. It indicates that Ras, Raf-1, MEK-1, and ERK-1/2 are involved in the process of intestinal fibrosis in CD rats. Moxibustion can downregulate the abnormal expression of colonic Ras, Raf-1, MEK-1, and ERK-1/2 protein and mRNA levels in CD intestinal fibrosis in rats. Moxibustion may play a role in the treatment of CD intestinal fibrosis by regulating ERK signaling pathway.

scholarly journals Pepsin-pancreatin protein hydrolysates from extruded amaranth inhibit markers of atherosclerosis in LPS-induced THP-1 macrophages-like human cells by reducing expression of proteins in LOX-1 signaling pathway

2014 ◽  
Vol 12 (1) ◽  
pp. 30 ◽  
Author(s):  
Alvaro Montoya-Rodríguez ◽  
Jorge Milán-Carrillo ◽  
Vermont P Dia ◽  
Cuauhtémoc Reyes-Moreno ◽  
Elvira González de Mejía
Keyword(s):  
Signaling Pathway ◽  
Protein Hydrolysates ◽  
Human Cells

scholarly journals Connexin 43 prevents the progression of diabetic renal tubulointerstitial fibrosis by regulating the SIRT1-HIF-1α signaling pathway

2020 ◽  
Vol 134 (13) ◽  
pp. 1573-1592
Author(s):  
Xiaohong Sun ◽  
Kaipeng Huang ◽  
Xiao Haiming ◽  
Zeyuan Lin ◽  
Yan Yang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Connexin 43 ◽  
Epithelial To Mesenchymal Transition ◽  
Hypoxia Inducible Factor ◽  
Pathological Process ◽  
Tubulointerstitial Fibrosis ◽  
Dependent Manner ◽  
Mesenchymal Transition ◽  
Renal Tubulointerstitial Fibrosis ◽  
Renal Tubular

Abstract Hyperglycemia-induced renal epithelial-to-mesenchymal transition (EMT) is a key pathological factor in diabetic renal tubulointerstitial fibrosis (RIF). Our previous studies have shown that connexin 43 (Cx43) activation attenuated the development of diabetic renal fibrosis. However, whether Cx43 regulates the EMT of renal tubular epithelial cells (TECs) and the pathological process of RIF under the diabetic conditions remains to be elucidated. In the present study, we identified that Cx43 protein expression was down-regulated in the kidney tissues of db/db mice as well as in high glucose (HG)-induced NRK-52E cells. Overexpression of Cx43 improved renal function in db/db spontaneous diabetic model mice, increased SIRT1 levels, decreased hypoxia-inducible factor (HIF)-1α expression, and reduced production of EMT markers and extracellular matrix (ECM) components. Additionally, Cx43 overexpression inhibited the EMT process and reduced the expression of ECM components such as fibronectin (FN), Collagen I, and Collagen IV in HG-induced NRK-52E cells, whereas Cx43 deficiency had the opposite effects. Mechanistically, Cx43 in a carboxyl-terminal signal transduction-dependent manner could up-regulate SIRT1 expression and enhance SIRT1-dependent deacetylation of HIF-1α to reduce HIF-1α activity, which eventually ameliorated renal EMT and diabetic RIF. Our study indicates the essential role of Cx43 in regulating renal EMT and diabetic RIF via regulating the SIRT1-HIF-1α signaling pathway and provides an experimental basis for Cx43 as a potential target for diabetic nephropathy (DN).

scholarly journals Echinacoside Improves Cognitive Impairment by Inhibiting Aβ Deposition Through the PI3K/AKT/Nrf2/PPARγ Signaling Pathways in APP/PS1 Mice

2021 ◽  
Author(s):  
hui qiu ◽  
min xue liu
Keyword(s):  
Signaling Pathway ◽  
Escape Latency ◽  
Senile Plaques ◽  
Pathological Process ◽  
Tnf Α ◽  
Nrf2 Signaling Pathway ◽  
Ros Formation ◽  
The Times ◽  
The Brain ◽  
Anti Inflammation

Abstract Echinacoside (ECH), a phenylethanoid glycoside, has protective activity in neurodegenerative disease, including anti-inflammation and antioxidation. However, the effects of ECH in Alzheimer’s disease (AD) are not very clear. This present study investigates the role and mechanism of ECH in the pathological process of AD. APP/PS1 mice were treated with ECH in 50 mg/kg/d for 3 months. Morris water maze, nesting test and immunofluorescence staining were used to observe whether ECH could improve AD pathology. Western blot was used to study the mechanism of ECH improving AD pathology. The results showed that ECH alleviated the memory impairment of APP/PS1 mice by reducing the time of escape latency as well as increasing the times of crossing the platform and rescued the impaired ability to construct nests. In addition, ECH significantly reduced the deposition of senile plaques in the brain and decreased the expression of BACE1 in APP/PS1 mice through activating PI3K/AKT/ Nrf2/PPARγ pathway. Furthermore, ECH decreased ROS formation, GP91 and 8-OHdG expression, upregulated the expression of SOD1 and SOD2 as well as activating the PI3K/AKT/Nrf2 signaling pathway. Moreover, ECH inhibited glia cells activation, pro-inflammatory cytokine IL-1β and TNF-α release, NLRP3 inflammasome formation through TXNIP/Trx-1 signaling pathway. In conclusion, this paper reported that ECH improved cognitive function, inhibited oxidative stress and inflammatory response in AD. Therefore, we suggest that ECH may be considered as a potential drug for AD treatment.

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