Abstract
Objective: The objective of this work is to investigate the histological and biochemical consequences of administering Dexmedetomidine (DEX), an alpha-2 adrenergic receptor agonist with notable sedative qualities as well as antioxidant and anti-inflammatory characteristics, in the context of Carbon tetrachloride (CCl4)-induced kidney injury.
Materials and Methods: The experimental design involved the random allocation of 30 Sprague-Dawley rats into three distinct groups. The experimental group designated as Group 1 received a single intraperitoneal administration of 1ml of saline solution containing 0.09% NaCl. Group 2 received an intraperitoneal injection of carbon tetrachloride (CCl4) at a dosage of 2 milliliters per kilogram. Group 3, referred to as the CCl4+Dexmedetomidine group, received a solitary intraperitoneal (i.p.) dosage of 100 µg/kg dexmedetomidine one hour before the intraperitoneal administration of 2mL/kg CCl4.
Results: Extensive necrosis and debris accumulation were observed in the tubules, particularly in the proximal tubules, within the CCl4-applied group. An elevation in malondialdehyde (MDA) concentrations and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) positivity, along with a reduction in glutathione (GSH) levels, was found in the renal tissues of the CCl4 experimental group as compared to the control group. In contrast, the CCl4+DEX group exhibited a reduction in the quantity of necrotic tubular cells, levels of MDA, and TUNEL positive. Additionally, there was an elevation in GSH levels compared to the group treated with CCl4 alone.
Conclusions: The administration of dexmedetomidine has been observed to potentially provide a protective effect against renal damage induced by CCl4. This phenomenon could potentially be linked to the modulation of tissue oxidative stress markers and the attenuation of apoptotic rate. The findings of our investigation provide evidence in favour of the utilization of dexmedetomidine as a promising therapeutic drug for mitigating renal injury.
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