## 4 Discussion  
Globally, stroke is a leading cause of mortality and disability and there are substantial economic costs for post-stroke care. Results from the 2015 iteration of the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) showed that although the age-standardised death rates and prevalence of stroke have decreased over time, the overall burden of stroke has remained high. The results provided here are the most up-to-date estimates of death, prevalence, incidence, and disability for overall stroke and the pathological types of ischaemic and haemorrhagic stroke [14; 15]. As a serious and complex pathological process, ischemia injury involves ion imbalance, peroxidation stress, neuroexcitotoxicity, and inflammatory activation. These cascading waterfall effects eventually lead to necrosis and apoptosis of nerve cells and the irreversible loss of nerve function [16; 17]. At present, the only effective treatment for cerebral ischemia in the medical community is thrombolysis. However, the window of time in which thrombol drugs can be used effectively limits their clinical applications [18]. Therefore, finding effective and reliable neuroprotective agents for stroke treatment is urgent. Clopidogrel, a platelet aggregation inhibitor, was reported to work as a stroke preventative drug  
Figure 8: The influence of BA on HIF-1\(\alpha\), AMPK, PPAR-\(\alpha\), PGC-1\(\alpha\), IxB\(\alpha\) and NF-kBp65 in OGD/R-induced SHSYSY cells. Compared with control cells (### \(p<0.001\)) and compared with OGD/R cells (** \(p<0.01\) and *** \(p<0.001\)). in vivo by slowing platelet aggregation [19]. The present study examined infarct size, cerebral edema, neurological behavior, and inflammatory cytokine levels of MCAO rats and OGD/R-induced SHSY5Y cells after BA intervention. Additionally, expression of the HIF-1\(\alpha\)/AMPK/PPAR\(\alpha\)/PGC-1\(\alpha\)/NF-\(\kappa\)B pathway was measured in animals and cells. Ischemia/reperfusion leads to cell inflammation caused by infiltration of immune cells [20]. Similarly, the acute stress response induced by inflammation may have a damaging effect on nerve cells [21]. The expression of inflammatory factors is mediated by activated NF-\(\kappa\)B, which is a key inflammatory regulator. After NF-\(\kappa\)B activation, inflammatory transcription factors migrate to the nucleus of a cell, promote pro-inflammatory gene transcription and enhance the inflammatory response [22]. The over-expression of PPAR and the PPAR activator rosiglitazone play important anti-inflammatory roles by inhibiting the NF-\(\kappa\)B signal pathway [23]. PPAR-\(\gamma\) coactivator-1\(\alpha\) (PGC-1\(\alpha\)) can also reduce the inflammatory effect by interfering with NF-\(\kappa\)B [24; 25]. HIF-1, a basic helix-loop-helix transcription factor, consists of two subunits, namely, HIF-1\(\alpha\) and HIF-1\(\beta\). Generally, HIF-1\(\alpha\) is a nuclear protein with transcriptional activity with a wide range of target gene profiles, including nearly 100 target genes related to hypoxia adaptation, inflammatory development, and tumor growth [26]. In hypoxic conditions, HIF-1\(\alpha\) degradation is inhibited, thereby increasing HIF-1\(\alpha\) levels [27]. Ischemic stroke was previously thought to result from hypoxia, which is associated with a decreased energy supply. The decreased adenosine triphosphate concentration, leading to a diminished energy supply, contributes to neuronal damage in cerebral ischemic injury [28]. AMPK controls the whole process of energy metabolism in tissues and cells; animals deficient in AMPK show accelerated energy failure and increased infarct sizes. When AMPK is activated, it rapidly phosphorylates downstream targets, blocks the ATP consumption pathway, and promotes activation of the ATP synthesis pathway [29; 30]. The association between HIF-1\(\alpha\) and AMPK is realized via sirtuin1 (SIRT1), which combines HIF-1\(\alpha\) and blocks the binding of p300 with HIF-1\(\alpha\)[31].