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Protective role of sitagliptin against oxidative stress in a kainic acid-induced status epilepticus in rats models via Nrf2/HO-1 pathway.
Drug Dev Res. 2019 06; 80(4):446-452.DD

Abstract

AIM

Sitagliptin (Sita) is a dipeptidyl peptidase-4 inhibitor which has been approved as a curing medicine for Type 2 diabetes (T2D) and has also reported its neuroprotective and antioxidant activity. This article describes the therapeutic effects of Sita on induced rat model of SE by kainic acid (KA) and investigated the antioxidative pathway of sita.

METHODS

Sprague-Dawley male rats were used randomly divided in four groups: vehicle control, KA and Sita + KA in a 5 and 10 mg/kg doses respectively in further groups. SE in rats was induced by the administration of KA in Phosphate buffered saline (PBS) intraperitoneally (IP) in a dose of 15 mg/kg. Seizure intensity, oxidative stress parameters, TUNEL assay, histopathology, and Nrf2/HO-1 expressions were evaluated.

RESULTS

Increment in the latency in SE results in delaying the initiation of disease in the pretreated rats by Sita compared to induce group (KA) as well the percentage of occurrence of SE was decreased. The content of MDA elevates whereas the SOD production decreases on administering the KA at various time intervals. Sita shows protective action against the KA-induced SE by reducing the oxidative stress thus inhibiting the change in SOD and MDA was observed after KA administration prior SE onset. Based on the above results, the study explains possible molecular mechanism of Sita. Sita Pretreatment showed significant elevation in expression of Nrf2 and HO-1 proteins in hippocampus region of the brain.

CONCLUSION

Above parameters defines the potential effect of Sita on brain injury occurred due to SE by anti-oxidative pathway.

Authors+Show Affiliations

Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.Biotech Center for Viral Disease Emergency, National Institute for Disease Control and Prevention, Chinese Disease Control and Prevention, Beijing, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30714645

Citation

Wang, Chong-Hao, and Na Zhu. "Protective Role of Sitagliptin Against Oxidative Stress in a Kainic Acid-induced Status Epilepticus in Rats Models Via Nrf2/HO-1 Pathway." Drug Development Research, vol. 80, no. 4, 2019, pp. 446-452.
Wang CH, Zhu N. Protective role of sitagliptin against oxidative stress in a kainic acid-induced status epilepticus in rats models via Nrf2/HO-1 pathway. Drug Dev Res. 2019;80(4):446-452.
Wang, C. H., & Zhu, N. (2019). Protective role of sitagliptin against oxidative stress in a kainic acid-induced status epilepticus in rats models via Nrf2/HO-1 pathway. Drug Development Research, 80(4), 446-452. https://doi.org/10.1002/ddr.21516
Wang CH, Zhu N. Protective Role of Sitagliptin Against Oxidative Stress in a Kainic Acid-induced Status Epilepticus in Rats Models Via Nrf2/HO-1 Pathway. Drug Dev Res. 2019;80(4):446-452. PubMed PMID: 30714645.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protective role of sitagliptin against oxidative stress in a kainic acid-induced status epilepticus in rats models via Nrf2/HO-1 pathway. AU - Wang,Chong-Hao, AU - Zhu,Na, Y1 - 2019/02/04/ PY - 2018/12/02/received PY - 2018/12/28/revised PY - 2019/01/09/accepted PY - 2019/2/5/pubmed PY - 2020/1/18/medline PY - 2019/2/5/entrez KW - HO-1 KW - Nrf2 KW - kainic acid KW - oxidative stress KW - sitagliptin SP - 446 EP - 452 JF - Drug development research JO - Drug Dev Res VL - 80 IS - 4 N2 - AIM: Sitagliptin (Sita) is a dipeptidyl peptidase-4 inhibitor which has been approved as a curing medicine for Type 2 diabetes (T2D) and has also reported its neuroprotective and antioxidant activity. This article describes the therapeutic effects of Sita on induced rat model of SE by kainic acid (KA) and investigated the antioxidative pathway of sita. METHODS: Sprague-Dawley male rats were used randomly divided in four groups: vehicle control, KA and Sita + KA in a 5 and 10 mg/kg doses respectively in further groups. SE in rats was induced by the administration of KA in Phosphate buffered saline (PBS) intraperitoneally (IP) in a dose of 15 mg/kg. Seizure intensity, oxidative stress parameters, TUNEL assay, histopathology, and Nrf2/HO-1 expressions were evaluated. RESULTS: Increment in the latency in SE results in delaying the initiation of disease in the pretreated rats by Sita compared to induce group (KA) as well the percentage of occurrence of SE was decreased. The content of MDA elevates whereas the SOD production decreases on administering the KA at various time intervals. Sita shows protective action against the KA-induced SE by reducing the oxidative stress thus inhibiting the change in SOD and MDA was observed after KA administration prior SE onset. Based on the above results, the study explains possible molecular mechanism of Sita. Sita Pretreatment showed significant elevation in expression of Nrf2 and HO-1 proteins in hippocampus region of the brain. CONCLUSION: Above parameters defines the potential effect of Sita on brain injury occurred due to SE by anti-oxidative pathway. SN - 1098-2299 UR - https://www.unboundmedicine.com/medline/citation/30714645/Protective_role_of_sitagliptin_against_oxidative_stress_in_a_kainic_acid_induced_status_epilepticus_in_rats_models_via_Nrf2/HO_1_pathway_ L2 - https://doi.org/10.1002/ddr.21516 DB - PRIME DP - Unbound Medicine ER -