Abstract
ObjectiveTo investigate the role of dexmedetomidine (DEX) in the inhibition of diabetic peripheral neuropathy (DPN) and the protection in the nerve damage.MethodsEighty male Sprague-Dawley (SD) rats were randomly allocated to four groups: the control group (C group), DPN model group (DPN group), DEX-treated group (DEX group), and the yohimbine treated group (YOH group). DPN was induced by intraperitoneal administration of streptozocin (STZ) (35 mg/kg). The body weights, blood glucose level, mechanical withdrawal threshold (MWT), thermal withdrawal latency (TWL), the motor, and sensory nerve conduction velocities (MNCV and SNCV) of sciatic nerve were measured. Then the sciatic nerve was isolated for H&E staining and immunohistochemical staining. The oxidative stress makers such as malondialdehyde (MDA), superoxide-dismutase (SOD), and glutathione peroxidase (GSH-Px) and apoptosis related cytokines such as Bax, Bcl-2, and caspase-3 were estimated.ResultsThere was no significant difference of the blood glucose and body weight among the DPN group, DEX group, and YOH group. H&E staining showed that DEX treatment can ameliorate the damage of sciatic nerve cells. In the DPN group, MWT, TWL, MNCV, and SNCV were significantly reduced compared with the C group (P < 0.05). In DEX group rats, MWT, TWL, MNCV, and SNCV were increased significantly (P < 0.05) compared with the DPN group and YOH group rats. Lower SOD and GSH-Px, and higher MDA were found in the DPN group compared with the C group (P < 0.01), and DEX treatment restored SOD, GSH-px, and MDA activity significantly (P < 0.01). The expression levels of Bax and caspase-3 were increased, while that of Bcl-2 was decreased significantly in the DPN group compared with the C group (P < 0.05). In the DEX group, the expression levels of Bax and caspase-3 were decreased significantly (P < 0.05), while that of Bcl-2 was increased significantly (P < 0.05) compared with the DPN group and the YOH group.ConclusionThe results of this study demonstrated that DEX has the inhibitory and protective effects on DPN of rats. This may be associated with its antioxidative and anti-apoptosis responses.
Highlights
Diabetic neuropathic pain is one of the most serious complications of diabetes mellitus (DM), which will afflict the quality of the patients’ life (Javed et al, 2019)
Recent work showed that hyperglycemia leads to excessive generation of superoxide anions in mitochondria and causes oxidative stress in tissue cells, which is a common mechanism leading to chronic complications of diabetes including diabetic peripheral neuropathy (DPN) (Vincent et al, 2004; Ziegler et al, 2004)
Stavniichuk (Stavniichuk et al, 2011) found that mitochondrial swelling, internal crest rupture, and typical apoptosis can change in the dorsal root ganglion (DRG) tissues of DM rats induced by streptozocin (STZ) at 12 weeks, and the expression of activated caspase-9 is increased
Summary
Diabetic neuropathic pain is one of the most serious complications of diabetes mellitus (DM), which will afflict the quality of the patients’ life (Javed et al, 2019). Recent work showed that hyperglycemia leads to excessive generation of superoxide anions in mitochondria and causes oxidative stress in tissue cells, which is a common mechanism leading to chronic complications of diabetes including DPN (Vincent et al, 2004; Ziegler et al, 2004). Stavniichuk (Stavniichuk et al, 2011) found that mitochondrial swelling, internal crest rupture, and typical apoptosis can change in the dorsal root ganglion (DRG) tissues of DM rats induced by streptozocin (STZ) at 12 weeks, and the expression of activated caspase-9 is increased. These mitochondrial changes were observed in sural nerve biopsies from patients with DPN. Oxidative stress regulating the apoptosis is considered to be an important factor in the occurrence of neuropathy
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