Ginsenoside RH1 Improves Neurological Function By Inhibiting Oxidative Stress and Promoting the Expression of Neurotrophic Factors in Cerebral Ischemia-Reperfusion Rats

Authors

  • Wang tian School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation, Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, Shandong, China
  • Zhang Guirong Shan Dong Yin Feng Academy of Life Science, Jinan, Shandong 250000, China
  • Wang Sensen School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation, Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, Shandong, China
  • Li Mingyue Shan Dong Yin Feng Academy of Life Science, Jinan, Shandong 250000, China
  • Zheng Qinpin School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation, Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, Shandong, China
  • Jia Xue School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation, Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, Shandong, China

DOI:

https://doi.org/10.22270/ajprd.v11i6.1324

Keywords:

Ginsenoside Rh1,Ischemic stroke,Neurological function,Oxidative stress

Abstract

Ginseng, a valued herb in China, showed efficacies for treatment or prevention of a series of conditions in patients. Ginsenoside Rh1 is the major active component of ginseng. The aim of this study was to investigate the neuroprotective effects of ginsenoside Rh1 on injury of cerebral ischemia-reperfusion in rats. Middle cerebral artery occlusion and reperfusion were performed in male Sprague-Dawley rats. The ischemic stroke rats were treated with ginsenoside Rh1 at dose of 5 mg/kg and 10 mg/kg by gavage. After 7-day treatment, neurological functions of animals were evaluated by adhesive removal tape and beam walking tests. Neuron injury was assessed by immunohistochemical staining. The levels of MDA, BDNF, NGF and activities of SOD, CAT in the ischemic hemisphere were assayed. Treatment with ginsenoside Rh1 for 7 days could significantly improve the neurological functions (P < 0.05)and increase the number of NeuN-positive cells in rats with cerebral ischemia(P < 0.01).Ginsenoside Rh1 decreased significantly MDA level(P < 0.01) and enhanced activitiesof SOD, CAT (P < 0.05 or P < 0.01).Further measurement showed that ginsenoside Rh1 also increased the levels of BDNF, NGF of the ischemic hemisphere(P<0.05 or P<0.01).The present findings demonstrated that ginsenoside Rh1 improved neurological function by inhibiting oxidative stress and promoting the expression of neurotrophic factors after cerebral ischemia-reperfusion.

 

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Author Biographies

Wang tian, School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation, Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, Shandong, China

School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation, Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, Shandong, China

Zhang Guirong, Shan Dong Yin Feng Academy of Life Science, Jinan, Shandong 250000, China

Shan Dong Yin Feng Academy of Life Science, Jinan, Shandong 250000, China

Wang Sensen, School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation, Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, Shandong, China

School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation, Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, Shandong, China

Li Mingyue, Shan Dong Yin Feng Academy of Life Science, Jinan, Shandong 250000, China

Shan Dong Yin Feng Academy of Life Science, Jinan, Shandong 250000, China

Zheng Qinpin, School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation, Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, Shandong, China

School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation, Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, Shandong, China

Jia Xue, School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation, Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, Shandong, China

School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation, Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, Shandong, China

References

Kuriakose D, Xiao Z. Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives. International journal of molecular sciences. 2020;21(20).

Yang C, Hawkins KE, Doré S, Candelario-Jalil E. Neuroinflammatory mechanisms of blood-brain barrier damage in ischemic stroke. American journal of physiology Cell physiology. 2019;316(2):C135-c53.

DeLong JH, Ohashi SN, O'Connor KC, Sansing LH. Inflammatory Responses After Ischemic Stroke. Seminars in immunopathology. 2022;44(5):625-48.

Orellana-Urzúa S, Rojas I, Líbano L, Rodrigo R. Pathophysiology of Ischemic Stroke: Role of Oxidative Stress. Current pharmaceutical design. 2020;26(34):4246-60.

Tsivgoulis G, Katsanos AH, Sandset EC, Turc G, Nguyen TN, Bivard A, et al. Thrombolysis for acute ischaemic stroke: current status and future perspectives. The Lancet Neurology. 2023;22(5):418-29.

Orellana-Urzúa S, Claps G, Rodrigo R. Improvement of a Novel Proposal for Antioxidant Treatment Against Brain Damage Occurring in Ischemic Stroke Patients. CNS & neurological disorders drug targets. 2021;20(1):3-21.

Sims SK, Wilken-Resman B, Smith CJ, Mitchell A, McGonegal L, Sims-Robinson C. Brain-Derived Neurotrophic Factor and Nerve Growth Factor Therapeutics for Brain Injury: The Current Translational Challenges in Preclinical and Clinical Research. Neural plasticity. 2022;2022:3889300.

Wei RL, Teng HJ, Yin B, Xu Y, Du Y, He FP, et al. A systematic review and meta-analysis of buyang huanwu decoction in animal model of focal cerebral ischemia. Evidence-based complementary and alternative medicine : eCAM. 2013;2013:138484.

Zhao X, He Y, Zhang Y, Wan H, Wan H, Yang J. Inhibition of Oxidative Stress: An Important Molecular Mechanism of Chinese Herbal Medicine (Astragalus membranaceus, Carthamus tinctorius L., Radix Salvia Miltiorrhizae, etc.) in the Treatment of Ischemic Stroke by Regulating the Antioxidant System. Oxidative medicine and cellular longevity. 2022;2022:1425369.

You L, Cha S, Kim MY, Cho JY. Ginsenosides are active ingredients in Panax ginseng with immunomodulatory properties from cellular to organismal levels. Journal of ginseng research. 2022;46(6):711-21.

Ni XC, Wang HF, Cai YY, Yang D, Alolga RN, Liu B, et al. Ginsenoside Rb1 inhibits astrocyte activation and promotes transfer of astrocytic mitochondria to neurons against ischemic stroke. Redox biology. 2022;54:102363.

Gao X, Zhang X, Cui L, Chen R, Zhang C, Xue J, et al. Ginsenoside Rb1 Promotes Motor Functional Recovery and Axonal Regeneration in Post-stroke Mice through cAMP/PKA/CREB Signaling Pathway. Brain research bulletin. 2020;154:51-60.

Chen J, Zhang X, Liu X, Zhang C, Shang W, Xue J, et al. Ginsenoside Rg1 promotes cerebral angiogenesis via the PI3K/Akt/mTOR signaling pathway in ischemic mice. European journal of pharmacology. 2019;856:172418.

Zhou Y, Li HQ, Lu L, Fu DL, Liu AJ, Li JH, et al. Ginsenoside Rg1 provides neuroprotection against blood brain barrier disruption and neurological injury in a rat model of cerebral ischemia/reperfusion through downregulation of aquaporin 4 expression. Phytomedicine : international journal of phytotherapy and phytopharmacology. 2014;21(7):998-1003.

Qiao X, He Y, Li W, Liu C, Yang J, Li H. 20(S)-Ginsenoside Rh1 inhibits cisplatin-induced hearing loss by inhibiting the MAPK signaling pathway and suppressing apoptosis in vitro. Biochimica et biophysica acta Molecular cell research. 2023;1870(5):119461.

Xu H, Jiang Y, Yu K, Zhang X, Shi Y. Effect of Ginsenoside Rh1 on Proliferation, Apoptosis, and Oxidative Stress in Vascular Endothelial Cells by Regulation of the Nuclear Erythroid 2-related Factor-2/Heme Oxygenase-1 Signaling Pathway. Journal of cardiovascular pharmacology. 2022;79(3):335-41.

Jin Y, Huynh DTN, Heo KS. Ginsenoside Rh1 inhibits tumor growth in MDA-MB-231 breast cancer cells via mitochondrial ROS and ER stress-mediated signaling pathway. Archives of pharmacal research. 2022;45(3):174-84.

Gai Y, Ma Z, Yu X, Qu S, Sui D. Effect of ginsenoside Rh1 on myocardial injury and heart function in isoproterenol-induced cardiotoxicity in rats. Toxicology mechanisms and methods. 2012;22(8):584-91.

Aspey BS, Taylor FL, Terruli M, Harrison MJ. Temporary middle cerebral artery occlusion in the rat: consistent protocol for a model of stroke and reperfusion. Neuropathology and applied neurobiology. 2000;26(3):232-42.

Yilmaz U, Tanbek K, Gul S, Gul M, Koc A, Sandal S. Melatonin Attenuates Cerebral Ischemia/Reperfusion Injury through Inducing Autophagy. Neuroendocrinology. 2023;113(10):1035-50.

Luong TN, Carlisle HJ, Southwell A, Patterson PH. Assessment of motor balance and coordination in mice using the balance beam. Journal of visualized experiments : JoVE. 2011(49).

Zhao Y, Zhang X, Chen X, Wei Y. Neuronal injuries in cerebral infarction and ischemic stroke: From mechanisms to treatment (Review). International journal of molecular medicine. 2022;49(2).

Che Y, Wang JF, Shao L, Young T. Oxidative damage to RNA but not DNA in the hippocampus of patients with major mental illness. Journal of psychiatry & neuroscience : JPN. 2010;35(5):296-302.

Cojocaru IM, Cojocaru M, Sapira V, Ionescu A. Evaluation of oxidative stress in patients with acute ischemic stroke. Romanian journal of internal medicine = Revue roumaine de medecine interne. 2013;51(2):97-106.

He L, He T, Farrar S, Ji L, Liu T, Ma X. Antioxidants Maintain Cellular Redox Homeostasis by Elimination of Reactive Oxygen Species. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology. 2017;44(2):532-53.

Zhu Y, Sun L, Huang T, Jia Y, Yang P, Zhang Q, et al. High Serum Brain-Derived Neurotrophic Factor Is Associated With Decreased Risks of Poor Prognosis After Ischemic Stroke. Stroke. 2023;54(7):1789-97.

Published

2023-12-15 — Updated on 2024-02-28

Versions

How to Cite

tian, W., Guirong, Z., Sensen, W., Mingyue, L., Qinpin, Z., & Xue, J. (2024). Ginsenoside RH1 Improves Neurological Function By Inhibiting Oxidative Stress and Promoting the Expression of Neurotrophic Factors in Cerebral Ischemia-Reperfusion Rats. Asian Journal of Pharmaceutical Research and Development, 11(6), 7–12. https://doi.org/10.22270/ajprd.v11i6.1324 (Original work published December 15, 2023)