Effects of polydatin from Huhuang Shaoshang Liniment on oxidative damage and inflammatory response in rats with cerebral ischemia-reperfusion.

OBJECTIVE

To analyze the effect of polydatin (PD) from Huhuang Shaoshang Liniment on oxidative damage and inflammatory response in rats with cerebral ischemia-reperfusion (CI/R), and the effect of PD on NF-E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1)/NAD(P)H quinone oxidoreductase 1 (NQO1) pathway.

METHODS

The rat model of focal CI/R was established using suture-occlusion method and treated with intraperitoneal injection of PD (25 mg/kg and 50 mg/kg). High performance liquid chromatography (HPLC) was used to determine the PD content in three batches of Huhuang Shaoshang Liniment. The neurological function scores of each group were observed at 24 h, 48 h, and 72 h postoperatively. The hematoxylin and eosin (HE) staining was conducted to observe the morphological structure of brain tissue, the triphenyltetrazolium chloride (TTC) staining was used to determine the size of cerebral infarction, and the neuronal apoptotic index was calculated using image analysis system under the optical microscope. The expressions of the Nrf2/HO-1/NQO1 pathway and neuronal apoptosis-related proteins in brain tissue were measured using Western blot.

RESULTS

The PD content in three batches of Huhuang Shaoshang Liniment was detected by HPLC, and the average result showed that the product contained 0.73 mg PD per 1 mL. The PD 50 mg/kg group and 25 mg/kg group showed lower neurological function scores at 24 h, 48 h, and 72 h postoperatively, lower percentage of cerebral infarction area on the ischemic side and apoptotic index, lower interleukin (IL)-1β, IL-6, malondialdehyde (MDA), and lactate dehydrogenase (LDH) levels, and lower Bax protein expression (P < 0.05), and showed higher IL-4, IL-10, superoxide dismutase (SOD), glutathione peroxidase (GPx), Nrf2, HO-1, NQO1, and c-Myc protein expression than the CI/R group (P < 0.05).

CONCLUSION

PD from Huhuang Shaoshang Liniment can alleviate neurological damage, improve neuronal morphology and structure, reduce cerebral infarction area, alleviate oxidative damage and inflammatory response, and inhibit neuronal cell apoptosis in CI/R model rats.