HBCOC attenuates cerebral ischemia-reperfusion injury in mice by inhibiting the inflammatory response and autophagy via TREM-1/ERK/NF-κB

We found that the HBCOC treatment alleviated nerve injury and reduced the cerebral infarction area caused by ischemia-reperfusion, simultaneously lowered the expression of IL-1β, IL-6, and TNF-α in plasma and brain tissues. HBCOC suppressed the levels of LC3II, lysosomes, and autophagy in the brain, suggesting potent inhibition of autophagy. Mechanistic analysis indicated that the expression of TREM-1/ERK/NF-κB pathway-related proteins and mRNA was higher in the saline group than that in the HBCOC group. HBCOC combined with the targeting TREM-1 receptor inhibitors LP17 inhibited the expression of the TREM-1 protein, further reducing the release of inflammatory factors and autophagy, restoring nerve function and infarct area after reperfusion, and exerting an overall protective effect against cerebral reperfusion injury. In summary, our results indicated that HBCOC alleviated cerebral ischemia-reperfusion injury in mice and inhibited inflammation and autophagy via TREM-1.