Evaluation of Antiparkinson’s activity of Ibuprofen and Monteleukast in 6 –Hydroxy Dopamine lesioned rat model

Y. Navya Reddy^a*, Nymisha Y^a, K. Rekha Rani^b, Kuruva Jyothirmai^b, T. Spurthi^d, Mohana Priya^c, R. Vadivelan^a
aDepartment of Pharmacology, JSS College of Pharmacy (JSS University, Mysore), Udhagamandalam, Tamilnadu, India -643001
^bDepartment of Pharmaceutics, CES College of Pharmacy, NH – 7, Chinnatekur, Kurnool, India – 518218.
^c Department of Pharmaceutical Chemistry, Dr. K.V Subbareddy Institute of Pharmacy, Lakshmipuram, Kurnool, India – 518218.
^dDepartment of Pharmacy Practice, CES College of Pharmacy, NH-7, Chinnatekur, Kurnool – 518218

A B S T R A C T
In our current study, we demonstrated the efficacy of Ibuprofen and Montelukast in order to alleviate or reduce neurodegeneration which cause neuronal death in Parkinson’s disease. Many recent reports are showing that Ibuprofen and Montelukast can be used as a potential drug in Parkinson’s disease, but these have not been properly worked out in preclinical testing. In our studies it was demonstrated that the complex I activity was significantly reduced for 6-OHDA control and in L-DOPA treated groups when compared to other treatment groups. It has been assumed that the ibuprofen and montelukast treatment may have some positive mechanism to normalize the complex I activity. Recent evidences suggested that the complex I abnormalities may induce apoptosis. Apoptosis refers to programmed cell death and was distinct from cell necrosis characteristically, morphologically and genetically. Morphological changes include chromatin condensation and the formation of chromatin bodies. Nuclear DNA undergoes extensive cleavage with the digestion of nucleosomes situated 180 base pairs of the part. The MT-ND5 gene provides instructions for making a protein called NADH dehydrogenase 5. This protein is part of a large enzyme complex known as complex I, which is active in mitochondria; our mitochondrial ND5 gene sequencing studies have revealed that mutations might have taken place in 6-OHDA induced Parkinson’s rat model and the results showed that the mutations might have been controlled with ibuprofen and montelukast treatment. The overall pharmacological evaluation explains a positive role of Ibuprofen and Montelukast in reducing neurodegeneration in 6-OHDA rat models.
Keywords: Parkinson’s disease, neurodegeneration, complex I, Ibuprofen, Montelukast