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Methylene blue attenuates mitochondrial dysfunction of rat kidney during experimental acute pancreatitis
Irma Kuliaviene1, Rasa Baniene2, Simona Virketyte2
1Department of Gastroenterology, Lithuanian University of Health Sciences, Kaunas, Lithuania.
Objective:
The disturbance of mitochondrial functions has been considered as one of the mechanisms of pathogenesis of acute pancreatitis (AP) followed by kidney failure. This study was aimed to investigate the effects of methylene blue (MB) on pancreas and kidney mitochondrial respiratory functions during experimental acute pancreatitis in rats.
Methods:
AP was induced by administrating sodium taurocholate into the pancreatic duct of male Wistar rats. The rats were divided into three groups: the MB group, MB (5 mg/kg) was injected intravenously 10 min prior to AP induction; the AP group, saline solution was injected intravenously 10 min prior to AP induction; and the sham operation group, isotonic sodium chlorine was used instead of sodium taurocholate. The animals were sacrificed after 24 h. The pancreas and kidney were removed for mitochondrial assay by oxygraphic and spectrophotometric methods.
Results:
Intravenous injection of MB did not prevent AP-induced inhibition of pancreatic mitochondrial respiration; however, MB significantly improved kidney mitochondrial respiratory functions with complex I-dependent substrates glutamate and malate. The activity of complex I of mitochondria isolated from AP-damaged kidney was increased after pretreatment with MB. However, MB did not affect AP-inhibited kidney mitochondrial respiration with succinate. MB had no protective effects on amylase activity or on urea content in serum in AP.
Conclusion:
The disturbances of kidney mitochondrial energy metabolism in experimental model of severe AP can be ameliorated by MB administration.
Insights
Methylene blue (MB) improved kidney mitochondrial function in rats with acute pancreatitis (AP), but did not protect the pancreas. This suggests MB may help mitigate kidney damage associated with AP.
Area of Science:
- Biochemistry
- Pathophysiology
- Pharmacology
Background:
- Mitochondrial dysfunction is implicated in acute pancreatitis (AP) pathogenesis and subsequent kidney failure.
- Investigating therapeutic agents that target mitochondrial function is crucial for managing AP complications.
Purpose of the Study:
- To evaluate the impact of methylene blue (MB) on pancreatic and kidney mitochondrial respiration in a rat model of AP.
- To determine if MB can ameliorate mitochondrial dysfunction in organs affected by AP.
Main Methods:
- Acute pancreatitis was induced in male Wistar rats using sodium taurocholate.
- Rats received intravenous methylene blue (MB) or saline prior to AP induction.
- Pancreas and kidney tissues were analyzed for mitochondrial respiratory function using oxygraphic and spectrophotometric assays.
Main Results:
- Methylene blue (MB) did not prevent AP-induced pancreatic mitochondrial respiration inhibition.
- MB significantly enhanced kidney mitochondrial respiration, particularly with complex I-dependent substrates (glutamate and malate).
- MB increased complex I activity in AP-damaged kidney mitochondria but did not affect respiration with succinate.
Conclusions:
- Methylene blue (MB) administration can ameliorate disturbances in kidney mitochondrial energy metabolism during experimental acute pancreatitis.
- MB shows potential as a therapeutic agent for kidney complications associated with severe AP.
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