Purpose
To examine the effects of quercetin on healing of experimental colon anastomosis injury in early and late period.
Methods
Eighty male Wistar-Albino rats were divided into 8 groups. For all groups, left colons of the rats were resected and for the rest end-to-end anastomosis was performed. Two of the groups for which the experiment protocol was ended on the 3rd and 7th day following the anastomosis were not administered with either quercetin or dimethylsulfoxide DMSO, whereas two other groups were administered with DMSO only, and four other groups were administered with quercetin dissolved in DMSO in doses of 20 and 100 mg/kg during the protocol. At the end of the study, anastomosis line was resected, histopathological evaluation was performed and bursting pressure, malondialdehyde, superoxide dismutase, catalase, and hydroxyproline levels were measured.
Results
Quercetin significantly increased hydroxyproline, superoxide dismutase, catalase levels, histopathological healing score, bursting pressure values and decreased malondialdehyde level in early period. It also significantly increased superoxide dismutase, catalase, and hydroxyproline levels and decreased malondialdehyde level in late period.
Conclusion
It was seen that quercetin speeds up the injury healing process and reveals an antioxidant effect, specifically in early period.
In recent years, hyperbaric oxygen (HBO2) therapy has been considered as an effective method for the treatment of gentamicin (GM)-induced renal toxicity. However, the findings related to the use of HBO2 for GM toxicity are limited and contradictory. The aim of this study is to investigate the protective role of HBO2 on GM-induced nephrotoxicity. For this purpose, Wistar albino rats (n=28) were randomly divided into four equal groups: C, HBO2, GM and GM+HBO2. GM (100 mg/kg, ip) and HBO2 were applied over seven days. On the eighth day blood and kidney tissue samples were harvested. The albumin, creatinine, and urea levels were determined from serum samples. Superoxide dismutase (SOD), glutathion peroxidase (GSH-Px) activities, malondialdehyde (MDA), total antioxidant status (TAS) and total oxidant status (TOS) values were analyzed spectrophotometrically. The relative expression level of TNF-α, IL-1β and Kim-1 gene were determined by qRT-PCR assays; histopathologic investigation was completed in kidney tissue samples. Serum urea, albumin and creatinine levels significantly increased in the GM group compared to the GM+HBO2 group. For antioxidant parameters the GM+HBO2 group was not statistically different from the C group but was significantly different compared with the GM group. TNF-α, IL-1β and Kim-1 gene expression levels in the GM group were statistically increased compared to the GM+HBO2 group (p=0.015, p=0.024, p=0.004) respectively. Severe tubular necrosis, epithelial desquamation and mild peritubular hemorrhage were observed in the GM-administrated group, while HBO2 exposure ameliorated these alterations. In conclusion, HBO2 exposure may be defined as a potential method for the prevention of GM-induced renal toxicity.
VPA is widely used in epilepsy and other psychological disorders, increasing the probability of developing non-alcoholic liver disease in long-term treatments. GLP-2 is a proglucagon belonging to the peptide family expressed in the intestine, pancreas and brain to date. Although there are many studies on the use of GLP-2 for therapeutic purposes on the gastrointestinal system, its effect on liver toxicity is unknown. We aimed to investigate the effect of GLP-2 administration on hepatic function in a rat model with VPA-induced hepatotoxicity. Rats were injected intraperitoneally at 500 mg/kg and GLP-2 5µg/kg a day. The rats (200-250g) were separated into four groups (n=7). Group C was administrated 1 mL of 0.9% SF, Group GLP treated with GLP-2 (5µg/kg/day), Group GLP+VPA were received GLP-2 (5µg/kg) 1 h prior to VPA (500 mg/kg), Group VPA received VPA (500 mg/kg), 1 h prior to 1 mL of 0.9% SF ip (n=7). Liver tissues were used to investigate effects of VPA and GLP-2 in the liver 15 days after application. While VPA caused moderate but significant liver damage according to biochemical results, mRNA expression of cytokines were found to significantly increase after the day 15. VPA administration significantly induced expression of Interleukin 1 beta (IL-1β), Tumor necrosis factor alpha (TNF-α), Interleukin 10 (IL-10). In contrast, GLP-2 treatment reduced expression of IL-1β, TNF-α and IL-10. Also malondialdehyde (MDA), glutathione s-transferase (α-GST), superoxide dismutase activities (SOD), total antioxidant status (TAS) and total oxidant status (TOS) levels were estimated. GLP-2 had positive effects on both liver enzymes and oxidative stress markers in VPA-induced hepatotoxicity. These results suggest that endogenous GLP-2 administration is associated with a mechanism that moderately protects liver tissue.
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