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Published on: April 16, 2019
Protective Assessment of Novel (BNC Formulation) against Brain Tumor
Anuradha Mishra1, Afza Ahmad2, Irfan Ahmad Ansari2
1Amity Institute of Pharmacy, Lucknow, Amity University Uttar Pradesh, Sector-125, Noida-201313, Uttar Pradesh, India.
Background:
Oxidative stress refers to non-homeostatic elevation within intracellular reactive oxygen species (ROS) levels and is associated with several neuro-related pathological conditions. Diclofenac is a commonly prescribed non-steroidal anti-inflammatory drug (NSAID) for treating aches and pain by reducing inflammation. Diclofenac is also associated with the induction of apoptotic cell death by altering the homeostatic balance within mitochondria. In the present report, the neuroprotective effects of BNC formulation constituted by Bacopa monnieri leaves, Nigella sativa and Curcuma longa rhizome seeds were investigated.
Methods:
The synthesized formulation was characterized using FT-IR and LC-MS along with organoleptic evaluation. Thereafter neuroprotective efficacy of BNC formulation was subsequently investigated against Diclofenac-induced oxidative stress in SH-SY5Y cells. The cells were pretreated with synthesized formulation and subsequently evaluated for amelioration in Diclofenac-induced cytotoxicity, and ROS augmentation. The neuroprotective effect of synthesized formulation was further explored by evaluating the changes in nuclear morphology, and apoptosis alleviation with concomitant regulatory effects on caspase-3 and -9 activation.
Results:
Diclofenac was found to be considerably cytotoxic against human neuroblastoma SHSY5Y cells. Intriguingly, Diclofenac-mediated toxicity was reduced significantly in SH-SY5Y cells pretreated with BNC formulation. Augmented ROS levels within Diclofenac-treated SHSY5Y cells were also reduced in the BNC formulation pretreated SH-SY5Y cells. Furthermore, BNC formulation pretreated SH-SY5Y cells also exhibited reduced dissipation of mitochondrial membrane potential, caspase-3 and -9, along with apoptosis after Diclofenac treatment.
Conclusion:
These findings indicated that, indeed, Diclofenac induces considerable ROSmediated apoptosis in SH-SY5Y cells, which further intriguingly ameliorated Diclofenacmediated cytotoxic effects on SH-SY5Y cells. This manuscript further collected information about available National and International patents published or granted in preparation of and thereof applications against motor and non-motor brain dysfunctions.
Insights
This study shows that a BNC formulation protects against Diclofenac-induced neurotoxicity by reducing reactive oxygen species (ROS) and apoptosis in brain cells. The BNC formulation offers neuroprotection against NSAID-induced damage.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Oxidative stress, an imbalance of reactive oxygen species (ROS), is linked to neurodegenerative diseases.
- Diclofenac, a non-steroidal anti-inflammatory drug (NSAID), can induce apoptosis by disrupting mitochondrial function.
- The neuroprotective potential of a BNC formulation (Bacopa monnieri, Nigella sativa, Curcuma longa) was investigated.
Purpose of the Study:
- To evaluate the neuroprotective effects of a novel BNC formulation.
- To investigate the BNC formulation's efficacy against Diclofenac-induced oxidative stress and apoptosis in neuronal cells.
- To explore the underlying mechanisms of neuroprotection offered by the BNC formulation.
Main Methods:
- Characterization of the BNC formulation using FT-IR, LC-MS, and organoleptic evaluation.
- Assessment of Diclofenac-induced cytotoxicity and ROS augmentation in SH-SY5Y cells.
- Evaluation of BNC formulation's impact on mitochondrial membrane potential, caspase activation, and apoptosis.
Main Results:
- Diclofenac demonstrated significant cytotoxicity and induced ROS in SH-SY5Y cells.
- Pretreatment with the BNC formulation significantly reduced Diclofenac-induced cytotoxicity and ROS levels.
- The BNC formulation mitigated apoptosis, preserved mitochondrial membrane potential, and regulated caspase-3 and -9 activation.
Conclusions:
- Diclofenac induces ROS-mediated apoptosis in SH-SY5Y cells.
- The BNC formulation effectively ameliorates Diclofenac-induced cytotoxic effects and neurotoxicity.
- This study provides evidence for the neuroprotective properties of the BNC formulation against NSAID-induced cellular damage.
