scholarly journals Integrated analysis of long noncoding RNAs and mRNA expression profiles reveals the potential role of lncRNAs in early stage of post-peripheral nerve injury in Sprague-Dawley rats

Aging ◽  
2021 ◽  
Author(s):  
Yujing Zhang ◽  
Zhaowei Zhu ◽  
Xiangxia Liu ◽  
Shuqia Xu ◽  
Yi Zhang ◽  
...  
1998 ◽  
Vol 62 (2) ◽  
pp. 228-235 ◽  
Author(s):  
Janice L Arruda ◽  
Raymond W Colburn ◽  
Amy J Rickman ◽  
Maria D Rutkowski ◽  
Joyce A DeLeo

2020 ◽  
Vol 135 ◽  
pp. 109470
Author(s):  
Florian S. Frueh ◽  
Epameinondas Gousopoulos ◽  
Dominic M. Power ◽  
Emmanuel Ampofo ◽  
Pietro Giovanoli ◽  
...  

2001 ◽  
Vol 280 (6) ◽  
pp. G1274-G1279 ◽  
Author(s):  
Eoin Waters ◽  
Jiang Huai Wang ◽  
H. Paul Redmond ◽  
Qiong Di Wu ◽  
Elaine Kay ◽  
...  

Acetaminophen overdose causes acute liver injury in both humans and animals. This study was designed to investigate the potential role of the conditionally essential amino acid taurine in preventing acetaminophen-induced hepatotoxicity. Male Sprague-Dawley rats were administered acetaminophen (800 mg/kg) intraperitoneally. Taurine (200 mg/kg) was given 12 h before, at the time of, and 1 or 2 h after acetaminophen injection. Acetaminophen treatment increased the plasma levels of aspartate transaminase, alanine aminotransferase, and alkaline phosphatase and caused hepatic DNA fragmentation and hepatocyte necrosis. Taurine administered before, simultaneously with, or 1 h after acetaminophen resulted in significant improvement in hepatic injury as represented by decrease of hepatocellular enzyme release and attenuation of hepatocyte apoptosis and necrosis, and this correlated with taurine-mediated attenuation of hepatic lipid peroxidation. These results indicate that taurine possesses prophylactic and therapeutic effects in acetaminophen-induced hepatic injury.


Author(s):  
Suk Peng Tang ◽  
Hasnan Jaafar ◽  
Siew Hua Gan ◽  
Kuttulebbai N.s. Sirajudeen ◽  
Siti Amrah Sulaiman

<p><strong>Objective: </strong>The objective of this research was to investigate the possible protective effect of Tualang honey (TH) in acute paraquat (PQ) toxicity in rats.</p><p><strong>Methods: </strong>A total of 48 male Sprague-Dawley rats aged eight weeks old were used. Oral PQ and TH were administered at 225 mg/kg and 0.2 g/kg, respectively. The effects of single and multiple TH treatmentson PQ-intoxicated rats were then investigated. Single TH treatment groups received TH at 0.5 (PQ+TH0.5h), 2 (PQ+TH2h) or 6 (PQ+TH6h) hours following PQ administration. Multiple TH treatment groups received TH at 0.5, 2 and 6 h (PQ+THtrp) or further daily treatment for the following six days (PQ+TH7d) after PQ administration (n=6 per group). The survival time of the rat was recorded until day 28 before sacrifice, which was followed by a histological examination.</p><p><strong>Results: </strong>Treatment with TH did not improve the survival rate of PQ-intoxicated rats. However, the median survival time of rats that received multiple TH treatments was significantly longer compared to that of the PQ+TH6h group. TH treatment was found to improve the histological outcomes of PQ-intoxicated rats, particularly in the lungs.</p><p><strong>Conclusion: </strong>Our findings suggest the potential role of honey in delaying the toxic effects of PQ.</p>


2017 ◽  
Vol 313 (3) ◽  
pp. F641-F656 ◽  
Author(s):  
Chuanming Xu ◽  
Aihua Lu ◽  
Hong Wang ◽  
Hui Fang ◽  
Li Zhou ◽  
...  

(Pro)renin receptor (PRR) is highly expressed in the distal nephron, but it has an unclear functional implication. The present study was conducted to explore a potential role of renal PRR during high K+ (HK) loading. In normal Sprague-Dawley rats, a 1-wk HK intake increased renal expression of full-length PRR and urinary excretion of soluble PRR (sPRR). Administration of PRO20, a decoy peptide antagonist of PRR, in K+-loaded animals elevated plasma K+ level and decreased urinary K+ excretion, accompanied with suppressed urinary aldosterone excretion and intrarenal aldosterone levels. HK downregulated Na+-Cl− cotransporter (NCC) expression but upregulated CYP11B2 (cytochrome P-450, family 11, subfamily B, polypeptide 2), renal outer medullary K+ channel (ROMK), calcium-activated potassium channel subunit α1 (α-BK), α-Na+-K+-ATPase (α-NKA), and epithelial Na+ channel subunit β (β-ENaC), all of which were blunted by PRO20. After HK loading was completed, urinary, but not plasma renin, was upregulated, which was blunted by PRO20. The same experiments that were performed using adrenalectomized (ADX) rats yielded similar results. Interestingly, spironolactone treatment in HK-loaded ADX rats attenuated kaliuresis but promoted natriuresis, which was associated with the suppressed responses of β-ENaC, α-NKA, ROMK, and α-BK protein expression. Taken together, we discovered a novel role of renal PRR in regulation of K+ homeostasis through a local mechanism involving intrarenal renin-angiotensin-aldosterone system and coordinated regulation of membrane Na+- and K+-transporting proteins.


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