scholarly journals Dry Needling of a Healthy Rat Achilles Tendon Increases Its Gene Expressions: A Pilot Study

Pain Medicine ◽  
2020 ◽  
Author(s):  
Laura Calderón-Díez ◽  
José Luis Sánchez-Sánchez ◽  
Javier Herrero-Turrión ◽  
Joshua Cleland ◽  
José L Arias-Buría ◽  
...  

Abstract Background Tendon dry needling is a potential treatment for tendinopathies. Several hypotheses have been proposed to explain its underlying mechanisms. No studies (to the best of our knowledge) have investigated changes in gene expression. Objective To investigate histological and gene expression changes after the application of dry needling to the healthy Achilles tendons of rats. Methods Six Sprague-Dawley male rats were randomly divided into two groups: no intervention or dry needling. Dry needling consisted of three sessions (once per week) to the Achilles tendon. Molecular expression of several genes involved in tendon repair and remodeling (e.g., Cox2, Mmp2, Mmp9, Col1a1, Col3a1, Vefg, and Scx) was assessed 7 days after the last needling session (day 28) or 28 days after for the no-intervention group. Histological tissue changes were determined with hematoxylin-eosin analyses. Results The hematoxylin-eosin–stained images revealed no substantial differences in collagen structure or the presence of inflammatory cells between the dry needling and no-intervention groups. A significant increase in the molecular expression of Cox2, Mmp2, Col3a1, and Scx genes was observed in Achilles tendons treated with dry needling when compared with the no-intervention group. Conclusion This animal pilot study found that the application of dry needling to the healthy Achilles tendons of rats is able to increase the expression of genes associated with collagen regeneration and tissue remodeling of the extracellular matrix with no further histological damage to the tendon.

2021 ◽  
Vol 120 ◽  
pp. 110384
Author(s):  
Sujata Khandare ◽  
Molly Smallcomb ◽  
Bailey Klein ◽  
Colby Geary ◽  
Julianna C. Simon ◽  
...  

2020 ◽  
Author(s):  
Kazim Sahin ◽  
Cemal ORHAN ◽  
Osman KUCUK ◽  
Mehmet TUZCU ◽  
Nurhan SAHIN ◽  
...  

Abstract Background: The objective of this work was to investigate the effects of a novel form of biotin (magnesium biotinate) at various levels on body weight, serum concentrations of glucose, insulin, cholesterol, and triglycerides, and liver expression of lipid metabolism-related genes such as SREBP-1c, FAS, AMPK-α1, ACC-1, ACC-2, PC, PCC and MCC in rats.Methods: A total of 42 male Sprague-Dawley rats were divided into six treatment groups and fed a standard diet-based egg white powdered diet supplemented with either commercial biotin (d-biotin) at 0.01, 1 or 100 mg/kg body weight or a novel form of biotin (magnesium biotinate) at 0.01, 1, or 100 mg/kg bodyweight for 35 days. The doses used at 0.01, 1 and 100 mg from each source represented a standard dietary dose (control), high dietary dose, and pharmacologic dose, respectively. Results: Bodyweight changes, feed intake, serum concentrations of glucose, insulin, creatine, and urea, and enzyme activities of ALT and AST were similar among treatments (P > 0.05). Serum total cholesterol and triglyceride concentrations of the rats decreased with biotin supplementation from both sources (P < 0.05). Concentrations were significantly lower with magnesium biotinate when comparing the 1 mg/kg dose groups (P < 0.05). Serum, liver, brain biotin concentrations, and liver cGMP contents were greater when rats were treated with magnesium biotinate versus d-biotin, particularly when comparing the 1 mg/kg and 100 mg/kg dose groups (P < 0.05). Both forms of biotin decreased the liver gene expression of SREBP‐1c and FAS and increased liver gene expression of AMPK-α1, ACC-1, ACC-2, PCC and MCC (P < 0.05). The magnitudes of responses were more emphasized with magnesium biotinate. Liver PC gene expression increased with biotin supplementation with no regard to dose or biotin form (P > 0.05).Conclusion: Results of the present work revealed that a new form of biotin, magnesium biotinate, compared with a commercial d-biotin, is more effective in reducing serum lipid concentrations and in regulating gene expressions of intermediary metabolism-related biomarkers.


2022 ◽  
Vol 8 ◽  
Author(s):  
I-Chen Li ◽  
Fang-Chia Chang ◽  
Ching-Chuan Kuo ◽  
Hsin-Tung Chu ◽  
Tsung-Ju Li ◽  
...  

Sleep disturbances have been the hallmark of the recent coronavirus disease 2019 pandemic. Studies have shown that once sleep is disrupted, it can lead to psychological and physical health issues which can, in turn, disrupt circadian rhythm and induce further sleep disruption. As consumers are trying to establish healthy routines, nutritional and preclinical safety investigation of fermented hispidin-enriched Sanghuangporus sanghuang mycelia (GKSS) as a novel food material for spontaneous sleep in Sprague-Dawley rats is conducted for the first time. Results showed that the nutritional analysis of GKSS including moisture, ash, crude lipid, crude protein, carbohydrate, and energy were found to be 2.4 ± 0.3%, 8.0 ± 2.5%, 1.7 ± 0.3%, 22.9 ± 1.2%, 65.1 ± 3.1%, and 367.1 ± 10.2 kcal/100 g respectively. In the 28-day repeated-dose oral toxicity study, only Sprague-Dawley male rats receiving 5 g/kg showed a slight decrease in feed consumption at week 3, but no associated clinical signs of toxicity or significant weight loss were observed. Although a significant reduction of the platelet count was found in mid- and high-dose GKSS treated male groups, such changes were noted to be within the normal range and were not correlated with relative spleen weight changes. Hence, the no observed adverse effect level (NOAEL) of GKSS was identified to be higher than 5 g/kg in rats. After the safety of GKSS is confirmed, the sleep-promoting effect of GKSS ethanolic extract enriched with hispidin was further assessed. Despite 75 mg/kg of GKSS ethanolic extract does not affect wakefulness, rapid eye movement (REM) sleep and non-REM (NREM) sleep, GKSS ethanolic extract at 150 mg/kg significantly decreased wakefulness and enhanced NREM and REM sleep. Interestingly, such effects seem to be mediated through anti-inflammatory activities via NF-E2-related factor-2 (Nrf2) signaling pathway. Taken together, these findings provide the preliminary evidence to studies support the claims suggesting that GKSS contained useful phytochemical hispidin could be considered as and is safe to use as a functional food agent or nutraceutical for relieving sleep problems mediated by Nrf2 pathway, which the results are useful for future clinical pilot study.


Author(s):  
Petra Stute ◽  
S. Ehrentraut ◽  
H.-H. Henneicke-von Zepelin ◽  
P. Nicken

Abstract Purpose This study aimed at assessing gene expression profiles in hippocampus and hypothalamus of ovariectomized (OVX) rats with or without treatment with an isopropanolic extract of Cimicifuga racemosa rhizomes (iCR) in comparison to intact rats. Methods Exploration of hippocampal (Hi) and hypothalamic (Hy) tissue from Sprague Dawley rats: without OVX (NHi = NHy = 4), tissues 3 months after OVX (NHi = 4, NHy = 3), or tissues of rats after their treatment with iCR for 3 months after OVX (NHi = NHy = 2). Gene expression profiles in these tissues were investigated by RNA-microarray-analysis and subsequent verification by qPCR. Results 4812 genes were differentially regulated when comparing the three groups in hippocampus and hypothalamus. iCR compensated the effects of OVX in 518 genes. This compensatory effect was most prominent in hippocampal signalling pathways, thereof genes (GAL, CALCA, HCRT, AVPR1A, PNOC, etc.) involved in thermoregulation, regulation of sleep and arousal, blood pressure regulation, metabolism, nociception, hormonal regulation, homeostasis, learning and cognition, mood regulation, neuroendocrine modulation, etc.. In the hypothalamus, iCR compensated OVX-effects at TAC3 and OPRM1 but not at KISS1. These genes are involved in the pathophysiology of hot flashes. Conclusions Our pilot study findings support a multifaceted mode of action of iCR in menopausal complaints on a tissue-specific brain gene expression level.


Author(s):  
Artur Pałasz ◽  
Piotr Żarczyński ◽  
Katarzyna Bogus ◽  
Kinga Mordecka-Chamera ◽  
Alessandra Della Vecchia ◽  
...  

Abstract Background Phoenixin, spexin and nesfatin-1 belong to a family of newly discovered multifunctional neuropeptides that play regulatory roles in several brain structures and modulate the activity of important neural networks. However, little is known about their expression and action at the level of brainstem. The present work was, therefore, focused on gene expression of the aforementioned peptides in the brainstem of rats chronically treated with olanzapine, a second generation antipsychotic drug. Methods Studies were carried out on adult, male Sprague–Dawley rats that were divided into 2 groups: control and experimental animals treated with olanzapine (28-day-long intraperitoneal injection, at dose 5 mg/kg daily). All individuals were killed under anesthesia and the brainstem excised. Total mRNA was isolated from homogenized samples of both structures and the RT-PCR method was used for estimation of related SMIM20/phoenixin, NPQ/spexin and NUCB2/nesfatin-1 gene expression. Results Long-term treatment with olanzapine is reflected in qualitatively different changes in expression of examined neuropeptides mRNA in the rat brainstem. Olanzapine significantly decreased NPQ/spexin mRNA expression, but increased SMIM20/phoenixin mRNA level in the rat brainstem; while NUCB2/nesfatin-1 mRNA expression remained unchanged. Conclusions Olanzapine can affect novel peptidergic signaling in the rat brainstem. This may cautiously suggest the presence of an alternative mode of its action.


Endocrinology ◽  
2021 ◽  
Author(s):  
Benjamin M Dungar ◽  
Chad D Schupbach ◽  
Jessie R Jacobson ◽  
Phillip G Kopf

Abstract Polybrominated diphenyl ethers (PBDEs) have been previously shown to alter various endocrine biosynthetic pathways. Growing epidemiological evidence suggests that PBDEs alter cardiovascular function. The goal of this study was to examine the effects of BDE-47 on adrenal corticosteroid pathways that play vital roles in cardiovascular homeostasis and pathophysiology. The effect of BDE-47 on aldosterone and cortisol secretion was characterized in a human adrenocortical cell line. HAC15 cells were exposed to various concentrations of BDE-47 (1 nM-100 μM). Cell viability, corticosteroid secretion, gene expression of enzymes involved in corticosteroid synthesis, and metabolic activity was examined. Additionally, Sprague Dawley male rats were orally exposed to BDE-47 (10 or 100 µg/kg), 5 days per week for 16 weeks. Organ weights and plasma corticosteroid levels were measured. In HAC15 cells, basal and stimulated aldosterone and cortisol secretion was significantly increased by BDE-47. Gene expression of several enzymes involved in corticosteroid synthesis and mitochondrial metabolism were also increased. In Sprague Dawley rats, adrenal, but not heart, kidney, or liver weights, were significantly increased in BDE-47 treatment groups. Plasma corticosterone levels were significantly increased in the 100 µg BDE-47/kg treatment group. No change in plasma aldosterone levels were observed with BDE-47 exposure. These data indicate that BDE-47 disrupts the regulation of corticosteroid secretion and provides further evidence that PBDEs are potential endocrine disruptors. Future studies will determine the underlying molecular mechanism of altered corticosteroid production and examine whether these alterations result in underlying cardiovascular disease in our rodent model of 16 week BDE-47 exposure.


2009 ◽  
Vol 30 (2) ◽  
pp. 81-89 ◽  
Author(s):  
María Del Mar Romero ◽  
José Antonio Fernández-López ◽  
Marià Alemany ◽  
Montserrat Esteve

We intended to determine how the liver copes with the massive handling of lipids induced by OE (oleoyl-oestrone), as well as to characterize and differentiate the actual OE effects from those that may be only the consequence of decreased food intake. Thus we used male rats treated with oral OE (10 nmol/g per day) compared with a vehicle only PF (pair-fed) group and controls fed ad libitum (vehicle only). Plasma parameters, and total liver lipids, glycogen, DNA and total mRNA were measured. RNA was extracted and used for real-time PCR analysis of the gene expression of enzymes and regulatory factors of liver energy metabolism. Most hepatic proteins showed similar gene expressions in OE and controls, but the differences widened between OE and PF rats, showing that OE effects could not be merely attributed to a lower energy intake. The liver of OE-treated rats largely maintained its ability to mobilize glucose for the synthesis of fats; this was achieved in part by a peculiar combination of regulative modifications that facilitate both fatty acid disposal and restrained glucose utilization under conditions of limited food supply but ample availability of internal energy stores. In conclusion, the results presented suggest that the effect of OE on liver metabolism may be (at least in part) mediated through an insulin-sensitivity-dependent modulation of the expression of SREBP-1c (sterol-regulatory-element-binding protein-1c), resulting in the unique combined effect of mildly increased (or maintained) glucose disposal but also limited enhancement of lipogenesis.


2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Evy Yulianti ◽  
Sunarti ◽  
Mae Sri Hartati Wahyuningsih

Abstract Background High glucose concentration increases the glycation process which leads to oxidative stress and inflammation, that can cause complications in diabetes. Several medicinal plants have been used in the treatment of diabetes and its complications. One of them is Kappaphycus alvarezii, an algae that has known antidiabetic abilities. This study aimed to examine the effect of K. alvarezii active fraction on plasma hydrogen peroxide (H2O2) and Tumor Necrosis Factor α (TNFα) levels, renal NADPH oxidase 4 (NOX4) and Nuclear Factor κ B (NFκB) gene expressions. Methods Active fraction was obtained from bioassay-guided fractionation with antiglycation ability. In vivo study was performed on twenty Wistar male rats. The level of H2O2 was measured using H2O2 Assay Kit, the Optical Density value measured using spectrophotometer at a wavelength of 405 nm. Plasma TNFα level was measured using ELISA. Renal NOX4 and NFκB gene expression was analyzed using qPCR. Results Active fraction significantly reduced plasma H2O2 but not TNFα levels. Furthermore, renal NOX4 gene expression was lower in the diabetic rat group treated with active fraction compared to the untreated group but not NFκB gene expression. Conclusions K. alvarezii active fraction has an activity to reduce plasma H2O2 as well as renal NOX4 gene expression. Therefore, this fraction could be developed as a potential candidate for diabetes treatment through oxidative stress mechanisms.


2020 ◽  
Author(s):  
Kazim Sahin ◽  
Cemal ORHAN ◽  
Osman KUCUK ◽  
Fusun Erten ◽  
Nurhan SAHIN ◽  
...  

Abstract Background: The objective of this work was to investigate the effects of a novel form of biotin (magnesium biotinate) at various levels on body weight, serum concentrations of glucose, insulin, cholesterol, and triglycerides, and liver expression of lipid metabolism-related genes such as SREBP-1c, FAS, AMPK-α1, ACC-1, ACC-2, PC, PCC and MCC in rats.Methods: A total of 42 male Sprague-Dawley rats were divided into six treatment groups and fed a standard diet-based egg white powdered diet supplemented with either commercial biotin (d-biotin) at 0.01, 1 or 100 mg/kg body weight or a novel form of biotin (magnesium biotinate) at 0.01, 1, or 100 mg/kg bodyweight for 35 days. The doses used at 0.01, 1 and 100 mg from each source represented a standard dietary dose (control), high dietary dose, and pharmacologic dose, respectively. Results: Bodyweight changes, feed intake, serum concentrations of glucose, insulin, creatine, and urea, and enzyme activities of ALT and AST were similar among treatments (P > 0.05). Serum total cholesterol and triglyceride concentrations of the rats decreased with biotin supplementation from both sources (P < 0.05). Concentrations were significantly lower with magnesium biotinate when comparing the 1 mg/kg dose groups (P < 0.05). Serum, liver, brain biotin concentrations, and liver cGMP contents were greater when rats were treated with magnesium biotinate versus d-biotin, particularly when comparing the 1 mg/kg and 100 mg/kg dose groups (P < 0.05). Both forms of biotin decreased the liver gene expression of SREBP‐1c and FAS and increased liver gene expression of AMPK-α1, ACC-1, ACC-2, PCC and MCC (P < 0.05). The magnitudes of responses were more emphasized with magnesium biotinate. Liver PC gene expression increased with biotin supplementation with no regard to dose or biotin form (P > 0.05).Conclusion: Results of the present work revealed that a new form of biotin, magnesium biotinate, compared with a commercial d-biotin, is more effective in reducing serum lipid concentrations and in regulating gene expressions of intermediary metabolism-related biomarkers.


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