Hypericum perforatum L. supplementation protects sciatic nerve injury-induced apoptotic, inflammatory and oxidative damage to muscle, blood and brain in rats

Abstract

HPL may play a role in preventing SNI-induced inflammatory, oxidative and apoptotic blood, muscle and brain damages through upregulation of the GSH and GPx values but downregulation of PARP, caspase level and cytokine production in SNI-induced rats.

Inhibition of the TRPM2 and TRPV1 Channels through Hypericum perforatum in Sciatic Nerve Injury-induced Rats Demonstrates their Key Role in Apoptosis and Mitochondrial Oxidative Stress of Sciatic Nerve and Dorsal Root Ganglion

“…Antioxidant and ROS scavenger effects of HP both in DRGN of SCI-induced rats (Uchida et al, 2008; Nazıroğlu et al, 2014a) and neutrophil of patients with inflammatory diseases (Nazıroğlu et al, 2014b,c) were reported. Recently, we observed modulator role of HP on apoptotic, inflammatory and oxidative stress values in muscle, blood and brain of SNI-induced rats (Uslusoy et al, 2017). Therefore, HP may attenuate oxidative stress, apoptosis and Ca 2+ entry through modulation of TRPM2 and TRPV1 in DRGN and sciatic neurons of SNI-induced rats.…”

Anti-inflammatory efficiency of erythropoietin in sciatic nerve damage

“…In another experimental study where especially the sciatic nerve damage was shown, it was observed that IL-1β levels significantly increased in trauma group compared to the control group [20][21][22]. In another study prepared based on sciatic nerve damage model, TNF-α, IL-1β, and IL-10 values increased significantly compared to the control group [6,3]. These markers cause neuroinflammationdependent cascade to start and worsen things after nerve damage.…”

“…IL-1β and TNF-α are important cytokines which are released from glial cells, and they play a key role in chronic pain, memory and damage pathogenesis. It was observed that sciatic nerve damage in the environment increased starting from the fifth hour following nerve damage [5,6,3]. Cytokines such as IL-1β and TNF-α were used to determine the anti-inflammatory effect in different experimental models.…”

“…The axonal structure is completely damaged by these histopathological changes, and the impulse transfer is destroyed in the first 48-96 hours following nerve injury [2]. The sciatic nerve, dorsal root ganglion, red blood cell and surrounding muscle tissue are affected by the damage [3]. Impulse cannot be transmitted to the muscle or sensory organs stimulated by the damaged nerve cell, and a neurological dysfunction develops depending on the affected area [4].Disruption of blood flow due to crushing over the nerve and the presence of reperfusion after the restoration of the damage causes the formation of acute phase reactants (cytokines such as TNF-α and IL-1β) and free oxygen radicals.…”

“…Impulse cannot be transmitted to the muscle or sensory organs stimulated by the damaged nerve cell, and a neurological dysfunction develops depending on the affected area [4].Disruption of blood flow due to crushing over the nerve and the presence of reperfusion after the restoration of the damage causes the formation of acute phase reactants (cytokines such as TNF-α and IL-1β) and free oxygen radicals. Furthermore, these cytokines that form in the neuro-inflammation cascade intensify the damage and result in myelin phagocytosis and the prevention of regeneration in damaged nerve cell [5,6].Although the efficiency of neurotrophic drugs, steroids, hormones, low dose radiation and different chemical materials in increasing nerve regeneration is reported today, and the highest level is technically reached in nerve repair with the development of microsurgical techniques, a total recovery cannot be provided in motor and sensory terms in nerve regeneration [1][2][3]7,8]. The peripheral nervous system is more successful in axonal regeneration as inhibitor myelin proteins are less dominant and Schwann cells are more active in distal.…”