Foeniculum vulgare
            (Fennel) promotes functional recovery and ameliorates oxidative stress following a lesion to the sciatic nerve in mouse model

Abstract Background Peripheral nerve injury is a debilitating condition that may lead to partial or complete motor, sensory and autonomic function loss and lacks effective therapy until date. Therefore, it is quite imperative to explore impending remedies for rapid and accurate functional retrieval following such conditions. Natural product-based intervention can prove effective to facilitate the process of functions regain. Methods Here, we investigated the effect of processed Strychnos nux-vomica seeds at a dose of 250 mg/kg body weight in a mouse model of induced Sciatic nerve lesion in promoting the recovery of the functions. A compression injury was induced in the Sciatic nerve of the right leg in the mice. Sensory function recovery was evaluated by hot-plate and formalin tests, whereas the motor function retrieval was assessed by measuring muscle grip strength, sciatic functional index, and muscle mass restoration. Oxidative stress and blood cell count were measured by biochemistry and haematological analyses. Results This study indicates that Strychnos nux-vomica seeds enhance the rate of recovery of both sensory and motor functions. It helps restore the muscle mass, attenuates total oxidant status and enhances the total anti-oxidant capacity of the biological system. Moreover, the treated animals manifested an enhanced glucose tolerance aptitude and augmented granulocyte and platelet counts. Improved oxidant control, enhanced glucose sensitivity and amended granulocyte and platelet counts are likely to contribute to the advantageous effects of Strychnos nux-vomica, and warrant further in-depth studies for deciphering possible mechanisms and identification of active constituent(s) responsible for these effects. Conclusion Strychnos nux-vomica seed offers functional recovery promoting effects following a mechanical injury to the Sciatic nerve and the possible reasons behind this effect can be reduced oxidative stress and improved glycaemic control. Further and detailed investigations can unravel this mystery.

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Basic neuroscience O-BN001. Calotropis procera (ROOT) ameliorates functions regain and attenuates oxidative stress in a mouse model of sciatic nerve compression injury

Clinical Neurophysiology ◽

10.1016/j.clinph.2021.02.159 ◽

2021 ◽

Vol 132 (8) ◽

pp. e77

Author(s):

Ghulam Hussain ◽

Azhar Rasul ◽

Haseeb Anwar ◽

Shoaib Ahmad Malik ◽

Shamaila Zafar ◽

...

Keyword(s):

Oxidative Stress ◽

Sciatic Nerve ◽

Mouse Model ◽

Nerve Compression ◽

Calotropis Procera ◽

Compression Injury ◽

Nerve Compression Injury

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Chitooligosaccharide Inhibits Scar Formation and Enhances Functional Recovery in a Mouse Model of Sciatic Nerve Injury

Molecular Neurobiology ◽

10.1007/s12035-015-9196-0 ◽

2015 ◽

Vol 53 (4) ◽

pp. 2249-2257 ◽

Cited By ~ 6

Author(s):

Hongping Hou ◽

Lihai Zhang ◽

Zuguang Ye ◽

Jianrong Li ◽

Zijian Lian ◽

...

Keyword(s):

Sciatic Nerve ◽

Mouse Model ◽

Nerve Injury ◽

Functional Recovery ◽

Scar Formation ◽

Sciatic Nerve Injury

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Microglia-Derived Exosomes Improve Spinal Cord Functional Recovery after Injury via Inhibiting Oxidative Stress and Promoting the Survival and Function of Endothelia Cells

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/1695087 ◽

2021 ◽

Vol 2021 ◽

pp. 1-16

Author(s):

Wei Peng ◽

Liyang Wan ◽

Zixiang Luo ◽

Yong Xie ◽

Yudong Liu ◽

...

Keyword(s):

Oxidative Stress ◽

Spinal Cord ◽

Mouse Model ◽

Functional Recovery ◽

Protein Levels ◽

Positive Effects ◽

Vascular Regeneration ◽

Cord Injury ◽

And Function

Traumatic spinal cord injury (SCI) is a devastating disease of the central nervous system with long-term disability and high mortality worldwide. Revascularization following SCI provides nutritional supports to rebuild and maintain the homeostasis of neuronal networks, and the subsequent promotion of angiogenesis is beneficial for functional recovery. Oxidative stress drastically produced following SCI has been contributed to endothelial dysfunction and the limited endogenous repair of microvasculature. Recently, exosomes, being regarded as potential therapeutic candidates for many kinds of diseases, have attracted great attentions due to its high bioavailability, safety, and stability. Microglia have been reported to exhibit proangiogenic function and guide the forming of vasculature during tissue repair. However, the specific role of microglia-derived exosomes (MG-Exos) played in SCI is still largely unknown. In the present study, we aimed to evaluate whether MG-Exos could protect spinal cord microvascular endothelial cells (SCMECs) against the toxic effects of oxidative stress, thus promote SCMECs’ survival and function. We also investigated the protective effects of MG-Exos in the mouse model of SCI to verify their capability. Our results demonstrated that MG-Exo treatment significantly decreased the level of oxidative stress (ROS), as well as did the protein levels of NOX2 when bEnd.3 cells were exposed to H2O2-induced oxidative stress in vitro and in vivo. Functional assays showed that MG-Exos could improve the survival and the ability of tube formation and migration in H2O2-induced bEnd.3 in vitro. Moreover, MG-Exos exhibited the positive effects on vascular regeneration and cell proliferation, as well as functional recovery, in the mouse model of SCI. Mechanically, the keap1/Nrf2/HO-1 signaling pathway was also investigated in order to unveil its molecular mechanism, and the results showed that MG-Exos could increase the protein levels of Nrf2 and HO-1 via inhibiting the keap1; they also triggered the expression of its downstream antioxidative-related genes, such as NQo1, Gclc, Cat, and Gsx1. Our findings indicated that MG-Exos exerted an antioxidant effect and positively modulated vascular regeneration and neurological functional recovery post-SCI by activating keap1/Nrf2/HO-1 signaling.

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