Possible mitigating effect of adropin on lung injury in diabetic rats: Targeting the role of Rho A/Rho-associated kinase pathway.
Fatma H RizkMervat H El-SakaRowida Raafat IbrahimOmnia Safwat El-DeebHoda A IbrahimAmira A El SaadanyShaimaa S MashalLeila AmmarAmal M AbdelsattarRamez A BarhomaPublished in: BioFactors (Oxford, England) (2023)
This study evaluated possible mitigating effect of adropin on lung injury in diabetic rats, targeting role of Rho A/Rho-associated kinase pathway. Rats were allocated into four groups: control, adropin, diabetic, and diabetic+adropin groups. At the termination of the experiment, serum fasting glucose, insulin and adropin levels and insulin resistance were calculated. Wet/dry ratio, histopathological, immunohistochemical analyses, and relative real time gene expression of lung tissue was determined. Interleukin-6, tumor necrosis factor alpha, malondialdehyde, 8-Oxo-2'-deoxyguanosine, reduced glutathione, superoxide dismutase, Bcl-2, BAX, myeloperoxidase, intracellular adhesion molecule-1, vascular cell adhesion molecule-1, and transforming growth factor-β were determined in lung tissue. Adropin treatment in diabetic rats notably attenuated hyperglycemia and insulin resistance. Also, it mitigated diabetic lung injury via suppressing effect on Rho A/ROCK pathway, apoptosis, inflammatory reactions, oxidative stress, and fibrosis of lung tissue. Adropin can be considered as a promising therapeutic agent for treating diabetic lung injury.
Keyphrases
- diabetic rats
- oxidative stress
- protein kinase
- type diabetes
- insulin resistance
- transforming growth factor
- induced apoptosis
- gene expression
- smooth muscle
- wound healing
- ischemia reperfusion injury
- cell adhesion
- dna damage
- metabolic syndrome
- adipose tissue
- cancer therapy
- endoplasmic reticulum stress
- high fat diet
- tyrosine kinase
- escherichia coli
- glycemic control
- pseudomonas aeruginosa
- skeletal muscle
- blood pressure
- cystic fibrosis
- staphylococcus aureus
- cell death
- hydrogen peroxide