Cerebral ischemic injury may lead to a series of serious brain diseases, death or different degrees of disability. Hypoxia‑inducible factor‑1α (HIF‑1α) is an oxygen‑sensitive transcription factor, which mediates the adaptive metabolic response to hypoxia and serves a key role in cerebral ischemia. HIF‑1α is the main molecule that responds to hypoxia. HIF‑1α serves an important role in the development of cerebral ischemia by participating in numerous processes, including metabolism, proliferation and angiogenesis. The present review focuses on the endogenous protective mechanism of cerebral ischemia and elaborates on the role of HIF‑1α in cerebral ischemia. In addition, it focuses on cerebral ischemia interventions that act on the HIF‑1α target, including biological factors, non‑coding RNA, hypoxic‑ischemic preconditioning and drugs, and expands upon the measures to strengthen the endogenous compensatory response to support HIF‑1α as a therapeutic target, thus providing novel suggestions for the treatment of cerebral ischemia.

The purpose of this study was to investigate the mechanism and effects of "Danggui-kushen" herb pair (DKHP) better than single drug in ischemic heart disease (IHD). IHD model was established by left anterior descending branch of coronary artery in rats. Rats were randomized into six groups and oral administration for 7 days: control, model, Danshen dripping pills (DS) (5.103 g/kg), Danggui (DG) (2.7 g/kg), Kushen (KS) (2.7 g/kg) and DKHP (2.7 g/kg). Electrocardiogram (ECG), myocardial infarction and damage assessment, histological inspection analysis, and various biochemical indexes of myocardial tissue were measured to evaluate the myocardial damage and the protective effects of drugs. The inflammatory levels were identified by HE staining and serum cytokine, and the expression of hypoxia-inducible factor 1α (HIF-1α), inhibitor kappa B kinaseβ (IKKβ) and nuclear transcription factor kappa B (NF-κB) were measured by immunohistochemistry. The results suggested that: compared with the control group, model group showed significantly myocardial tissue abnormalities, and increased levels of inflammatory cytokine. Treatment with drugs inhibited the increase of α-hydroxybutyrate dehydrogenase (α-HBDH), creatine kinase (CK), creatinekinase isoenzyme (CK-MB), interleukin 1 (IL-1) and interleukin 6 (IL-6). The results of immunohistochemical showed that drugs-treatment inhibited the expression of IKKβ and the P-p65, increased the expression of HIF-1α, which demonstrated that the anti-inflammatory effects of DKHP was achieved by suppressing of NF-κB signaling. These observations indicated that DKHP can ameliorate myocardial injury better than single. And these are related to the inhibition of NF-κB and actives HIF-1α signaling.

Oxidative stress, which is caused by Amyloid-β deposition in brain, plays an important role in Alzheimer’s disease. In this study, we found that lignans from Schisandra chinensis rattan stems (rsSCH-L) could reduce the escape latency and the distance travelled by the Aβ_1–42 injected rats while the crossing platform time was enhanced in the Morris water maze test. Further research demonstrated that lignans from rsSCH-L attenuated Aβ_1-42-induced neuronal cell injury by increasing the content of SOD and GSH-Px and decreasing the levels of LDH, ROS, and MDA. Moreover, rsSCH-L also inhibited the apoptosis of primary neuronal cells. The mechanisms of the apoptosis were related with the downregulation of caspase-3, caspase-8, Bax, and upregulation of Bcl-2. Taken together, the results show that rsSCH-L can improve cognitive ability in vivo. Meanwhile rsSCH-L exhibit a neuroprotective environment against oxidative stress and apoptosis in vitro. Therefore, rsSCH-L may be a potential therapeutic agent for this neurodegenerative disease.