The Protective Effect and Mechanism of Dexmedetomidine on Diabetic Peripheral Neuropathy in Rats

Abstract

Objective: To investigate the role of dexmedetomidine (DEX) in the inhibition of diabetic peripheral neuropathy (DPN) and the protection in the nerve damage. Methods: Eighty 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. Results: There 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. Conclusion: The 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 antiapoptosis responses.

Oleuropein Improves Cognitive Dysfunction and Neuroinflammation in Diabetic Rats through the PI3K/Akt/mTOR Pathway

“…At present, many antidiabetic drugs have been used clinically to treat DM. However, existing antidiabetic drugs are ineffective for their complications [ 18 ], including cognitive impairment, and even have had gastrointestinal side effects, such as nausea, vomiting, diarrhea, and lactic acidosis [ 19 ]. Therefore, there is a need to find a natural-derived drug with good curative effects and few side effects for the treatment of diabetes.…”

The Effect of Yiqi Huoxue Tongluo Decoction on Spinal Cord Microglia Activation and ASK1-MKK3-p38 Signal Pathway in Rats with Diabetic Neuropathic Pain

“…DNP is a chronic low-grade neuroinflammatory response [ 18 , 19 ]. An effective DNP model can be established by STZ.…”

[Retracted] Lidocaine Ameliorates Diabetic Peripheral Neuropathy in Streptozotocin‐Induced Diabetic Rats through Modulating the c‐Jun Signaling Pathway

“…MWT and thermal latency (TML) are measured as described previously [ 24 ]. In brief, the BME-410C automatic thermal pain stimulator is used to irradiate the plantar part of rats.…”

“…However, there is no report that the effect of lidocaine on DPN is related to the expression of the c-Jun signaling pathway. Therefore, the purpose of this study is to observe the therapeutic effect of lidocaine on DPN rats and then to explore the correlation between the effect of lidocaine on the c-Jun signal pathway and DPN treatment [ 24 ]. The research results can provide a new experimental basis for lidocaine in the treatment of DPN.…”