Qualification: 
Ph.D, M. Pharm., B. Pham.
athirakv@aims.amrita.edu

Athira K. V. joined in the Department of Pharmacology at Amrita School of Pharmacy in July 2018. She pursued graduation in Pharmacy from College of Pharmaceutical Sciences, Medical College, Thiruvananthapuram, Kerala and post-graduation as well as Ph. D. from National Institute of Pharmaceutical Education and Research (NIPER), Guwahati, Assam.

She has won several awards and fellowships during her studies and has published several papers in reputed journals.

Awards and Fellowships

  • First prize in oral presentation at Inter-NIPER scientific, sports & cultural meet SPARDHA-2018 at NIPER S.A.S. Nagar, Mohali.
  • Second prize in oral presentation at North East Pharmaceutical Convention (NEPC)-2017, Guwahati.
  • INSA-CSIR-DAE/BRNS-CICS Travel Fellowship to attend International Congress of Immunology (ICI)-2016, Melbourne.
  • Category 1 list, Biotechnology Eligibility Test (BET), 2014 for DBT- JRFProgramme.
  • First prize in oral presentation, Association of Oncologists of Northeast India (AONEI)- 2014 at Guwahati.

Publications

Publication Type: Book Chapter

Year of Publication Title

2018

Athira K V, Samudrala, P. K., and Lahkar, M., “Molecular mechanism of the flavonoids against kidney disorders”, in Recent advances in the molecular mechanism of flavonoids, Studium Press, 2018.

Publication Type: Journal Article

Year of Publication Title

2018

Athira K V, Rajaram Mohanrao Madhana, Indu Chandran JS, Mangala Lahkar, Swapnil Sinha, and V.G.M. Naidu, “Antidepressant activity of vorinostat is associated with amelioration of oxidative stress and inflammation in a corticosterone-induced chronic stress model in mice”, Behavioural Brain Research, vol. 344, pp. 73 - 84, 2018.[Abstract]


Major depressive disorder (MDD) is a multifactorial neuropsychiatric disorder. Chronic administration of corticosterone (CORT) to rodents is used to mimic the stress associated dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, a well-established feature found in depressive patients. Recently, preclinical studies have demonstrated the antidepressant potential of histone deacetylase (HDAC) inhibitors. So, we examined the antidepressant potential of vorinostat (VOR), a HDAC inhibitor against CORT injections in male mice. VOR (25 mg/kg; intraperitoneal) and fluoxetine (FLX) (15 mg/kg; oral) treatments were provided to CORT administered mice. At the end of dosing schedule, neurobehavioral tests were conducted; followed by mechanistic evaluation through biochemical analysis, RTPCR and western blot in serum and hippocampus. Neurobehavioral tests revealed the development of anxiety/depressive-like behavior in CORT mice as compared to the vehicle control. Depressive-mice showed concomitant HPA axis dysregulation as observed from the significant increase in serum CORT and ACTH. Chronic CORT administration was found to significantly increase hippocampal malondialdehyde (MDA) and iNOS levels while lowering glutathione (GSH) content, as compared to vehicle control. VOR treatment, in a similar manner to the classical antidepressant FLX, significantly ameliorated anxiety/depressive-like behavior along with HPA axis alterations induced by CORT. The antidepressant-like ability of drug treatments against chronic CORT induced stress model, as revealed in our study, may be due to their potential to mitigate inflammatory damage and oxidative stress via modulation of hippocampal NF-κB p65, COX-2, HDAC2 and phosphorylated JNK levels.

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2016

C. S. Sriram, Jangra, A., Bezbaruah, B. K., Athira K V, and Sykam, S., “Alternative mechanisms of inhibiting activity of poly (ADP-ribose) polymerase-1”, Frontiers in Bioscience, vol. 8, pp. 123-128, 2016.

2016

Athira K V, Rajaram Mohanrao Madhana, and Mangala Lahkar, “Flavonoids, the emerging dietary supplement against cisplatin-induced nephrotoxicity”, Chemico-Biological Interactions, vol. 248, pp. 18 - 20, 2016.[Abstract]


The letter illustrates the emerging potential of flavonoids as dietary supplement to ameliorate cisplatin-induced nephrotoxicity and refers to the recent article on ‘‘Anti-apoptotic and anti-inflammatory effects of naringin on cisplatin-induced renal injury in the rat’’ by Chtourou et al. They demonstrated that supplementation of naringin, a flavanone glycoside, found in grape and citrus fruit species, can attenuate cisplatin-induced renal dysfunction via restoration of redox balance and suppression of inflammation, NF-κB activation and apoptosis. The chemotherapeutic efficacy of cisplatin has always compelled the researchers to find solution to ameliorate its side effects. In recent years, numerous candidates have been evaluated for their protective potential against cisplatin-induced nephrotoxicity and flavonoids have come up with promising results. The future prospects might be promising with a proper refinement and collective integration of the preclinical and clinical research in the field of flavonoid supplementation to cisplatin therapy.

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2016

Athira K V, Madhana, R. Mohanrao, Kasala, E. Reddy, Samudrala, P. Kumar, Lahkar, M., and Gogoi, R., “Morin Hydrate Mitigates Cisplatin-Induced Renal and Hepatic Injury by Impeding Oxidative/Nitrosative Stress and Inflammation in Mice”, Journal of biochemical and molecular toxicology, vol. 30, pp. 571–579, 2016.[Abstract]


Cisplatin is a widely used chemotherapeutic drug; however, it induces damage on kidney and liver at clinically effective higher doses. Morin hydrate possesses antioxidant, anti‐inflammatory, and anticancer properties. Therefore, we aimed to investigate the effects of morin hydrate (50 and 100 mg/kg, orally) against the renohepatic toxicity induced by a high dose of cisplatin (20 mg/kg, intraperitoneally). Renal and hepatic function, oxidative/nitrosative stress, and inflammatory markers along with histopathology were evaluated. Morin hydrate ameliorated cisplatin‐induced renohepatic toxicity significantly at 100 mg/kg as evidenced from the significant reversal of cisplatin‐induced body weight loss, mortality, functional and structural alterations of kidney, and liver. The protective role offered by morin hydrate against cisplatin‐induced renohepatic toxicity is by virtue of its free radical scavenging property, thereby abating the depletion of cellular antioxidant defense components and through modulation of inflammatory cytokines. We speculate morin hydrate as a protective candidate against renohepatic toxicity of cisplatin.

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2015

E. Reddy Kasala, Bodduluru, L. Narendra, Madana, R. Mohanrao, Athira K V, Gogoi, R., and Barua, C. C., “Chemopreventive and therapeutic potential of chrysin in cancer: mechanistic perspectives”, Toxicology Letters, vol. 233, pp. 214 - 225, 2015.[Abstract]


Chrysin, a naturally occurring flavone, abundantly found in numerous plant extracts including propolis and in honey is one of the most widely used herbal medicine in Asian countries. Nowadays, chrysin has become the foremost candidate exhibiting health benefits, owing to its multiple bioactivities such as antioxidant, anti-inflammatory, anti-allergic, anti-diabetic, anti-estrogenic, antibacterial and antitumor activities. Anticancer activity is most promising among the multiple pharmacological effects displayed by chrysin. In vitro and in vivo models have shown that chrysin inhibits cancer growth through induction of apoptosis, alteration of cell cycle and inhibition of angiogenesis, invasion and metastasis without causing any toxicity and undesirable side effects to normal cells. Chrysin displays these effects through selective modulation of multiple cell signaling pathways which are linked to inflammation, survival, growth, angiogenesis, invasion and metastasis of cancer cells. This broad spectrum of antitumor activity in conjunction with low toxicity underscores the translational value of chrysin in cancer therapy. The present review highlights the chemopreventive and therapeutic effects, molecular targets and antineoplastic mechanisms that contribute to the observed anticancer activity of chrysin.

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2015

A. Jangra, Kasbe, P., Pandey, S. Narayan, Dwivedi, S., Gurjar, S. S., Kwatra, M., Mishra, M., Athira K V, Sulakhiya, K., Gogoi, R., Sarma, N., Bezbaruah, B. K., and Lahkar, M., “Hesperidin and Silibinin Ameliorate Aluminum-Induced Neurotoxicity: Modulation of Antioxidants and Inflammatory Cytokines Level in Mice Hippocampus”, Biological Trace Element Research, vol. 168, pp. 462–471, 2015.[Abstract]


Mounting evidence suggests that long-term aluminum exposure results in severe toxic effects, including neurobehavioral and neurochemical anomalies. The present study was performed to examine the neuroprotective potential of hesperidin and silibinin against aluminum chloride (AlCl3)-induced neurotoxicity in mice. AlCl3 (100 mg/kg/day) was injected daily through oral gavage for 42 days. Concomitantly, hesperidin (50 and 100 mg/kg/day, p.o.) and silibinin (100 and 200 mg/kg/day, p.o.) was administered for 42 days in different groups. The extent of cognitive impairment was assessed by Morris water maze and novel object recognition test on the 43rd day. Neurotoxicity was assessed by measuring oxido-nitrosative stress and proinflammatory cytokines in the hippocampus of mice. Six weeks treatment with AlCl3 caused cognitive impairment as indicated by an increase in the retention latency time and reduction in the percentage of recognition index. AlCl3-treated group showed oxido-nitrosative stress as indicated by increase in the level of lipid peroxidation, nitrite and depleted reduced glutathione, catalase activity in the hippocampus. Moreover, the chronic AlCl3 administration raised the proinflammatory cytokines (interleukin-1$\beta$ and tumor necrosis factor-$\alpha$) level and increased acetylcholinesterase activity and reduced the BDNF content in the hippocampus of AlCl3-treated animals. However, chronic treatment with hesperidin and silibinin at higher doses significantly ameliorated the AlCl3-induced cognitive impairment and hippocampal biochemical anomalies. The present study clearly indicated that hesperidin and silibinin exert neuroprotective effects against AlCl3-induced cognitive impairment and neurochemical changes. Amelioration of cognitive impairment may be attributed to the impediment of oxido-nitrosative stress and inflammation in the hippocampus.

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2015

S. Hamid Ali, Rajaram Mohanrao Madhana, Athira K V, Kasala, E. Reddy, Bodduluru, L. Narendra, Pitta, S., Mahareddy, J. Reddy, and Mangala Lahkar, “Resveratrol ameliorates depressive-like behavior in repeated corticosterone-induced depression in mice”, Steroids, vol. 101, pp. 37 - 42, 2015.[Abstract]


A mouse model of depression has been recently developed by exogenous corticosterone (CORT) administration, which has shown to mimic HPA-axis induced depression-like state in animals. The present study aimed to examine the antidepressant-like effect and the possible mechanisms of resveratrol, a naturally occurring polyphenol of phytoalexin family, on depressive-like behavior induced by repeated corticosterone injections in mice. Mice were injected subcutaneously (s.c.) with 40mg/kg corticosterone (CORT) chronically for 21days. Resveratrol and fluoxetine were administered 30min prior to the CORT injection. After 21-days treatment with respective drugs, behavioral and biochemical parameters were estimated. Since brain derived neurotrophic factor (BDNF) has been implicated in antidepressant activity of many drugs, we also evaluated the effect of resveratrol on BDNF in the hippocampus. Three weeks of CORT injections in mice resulted in depressive-like behavior, as indicated by the significant decrease in sucrose consumption and increase in immobility time in the forced swim test and tail suspension test. Further, there was a significant increase in serum corticosterone level and a significant decrease in hippocampus BDNF level in CORT-treated mice. Treatment of mice with resveratrol significantly ameliorated all the behavioral and biochemical changes induced by corticosterone. These results suggest that resveratrol produces an antidepressant-like effect in CORT-induced depression in mice, which is possibly mediated by rectifying the stress-based hypothalamic–pituitary–adrenal (HPA) axis dysfunction paradigm and upregulation of hippocampal BDNF levels.

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