Protective effects of beef decoction rich in carnosine on cerebral ischemia injury by permanent middle cerebral artery occlusion in rats
- Ai‑Hong Wang
- Qian Ma
- Xin Wang
- Gui‑Hua Xu
Published online on: November 17, 2017
Copyright: © Wang et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
Inflammation has a role in the cerebral injury induced by ischemia and the present study aimed to determine the mechanism of the protective effect of beef decoction (BD) with carnosine against it. A rat model of permanent middle cerebral artery occlusion was established using a suture method in the vehicle and each of the BD groups. In experiment 1, 72 Sprague Dawley (SD) rats were randomly divided into three groups: Sham, vehicle and BD‑treated group. Rats in the BD group were given 600 mg/kg BD by oral gavage for 1, 3 and 7 days. The sham and vehicle group rats received an equivalent amount of normal saline. In experiment 2, 60 SD rats were randomly divided into six groups: Sham‑operated I, sham‑operated II, vehicle, low‑dose BD, medium‑dose BD and high‑dose BD group. Rats in the low‑, medium‑ and high‑dose BD groups were given BD at the dose of 200, 400 and 600 mg/kg, respectively, by oral gavage for 7 days. Rats in the sham‑operated II group were given 600 mg/kg BD. Rats in the sham‑operated I group and vehicle group were given the same volume of normal saline by oral gavage. The body weight, neurological deficits and infarct volume were recorded at 1, 3 and 7 days after the operation. Furthermore, the effect of different doses of BD on interleukin‑6 (IL‑6), tumor necrosis factor‑α (TNF‑α), interferon‑γ (IFN‑γ) and interleukin‑4 (IL‑4) levels in peripheral blood was measured at 7 days. BD‑treated rats showed less neurological deficits and a smaller infarct volume at 7 days. BD at 400 and 600 mg/kg significantly decreased the infarct volume in rats. At 600 mg/kg BD, a decline in IL‑6, TNF‑α, IFN‑γ and an increase in IL‑4 expression was observed in the BD groups, while no difference in body weight and neurological dysfunction was detected. In conclusion, BD is a neuroprotective agent that may be used as a supplement treatment of ischemic stroke.