Cor pulmonale (pulmonary heart disease) is a chronic progressive complicated disease for which treatment needs to be sustained all the time, creating a great financial burden on individuals and society. In order to improve the life quality of cor pulmonale patients and decrease the dosage and quantity of the routine treatment, in China, TCM is often administered to patients with cor pulmonale. The results of many clinical trials have indicated that Salvia miltiorrhiza and complex Salvia miltiorrhiza injection may be an alternative medicine for cor pulmonale. With the purpose to prove whether Salvia miltiorrhiza and complex Salvia miltiorrhiza benefit the cor pulmonale patients, respectively, we carried out a systematic review to evaluate the efficacy and safety of Salvia miltiorrhiza and complex Salvia miltiorrhiza injection in cor pulmonale patients. Overall, 2,715 patients were identified from 35 randomized controlled trials. The meta-analysis used I(2) test for heterogeneity and chose random or fixed model according to heterogeneity of included studies. Clinical outcomes were evaluated by total effectiveness rate, partial pressure of oxygen ( PaO 2) and carbon dioxide ( PaCO 2), hemorheology, mPAP and adverse effects. Compared with routine medicine treatment alone, routine medicine treatment plus Salvia miltiorrhiza or complex Salvia miltiorrhiza injection showed better outcomes: A significantly higher clinical effectiveness rate ratio (p < 0.001), increase in PaO 2 (p < 0.001) and decrease in PaCO 2 (p < 0.001), improvement in hemorheology (p < 0.001), and alleviation in mPAP (p < 0.05). There is no obvious adverse effect reported. In summary, there are some evidences suggesting that Salvia miltiorrhiza or complex Salvia miltiorrhiza injection are active in cor pulmonale, however, the results were limited by the methodological flaws of the included studies. Long-term and high quality clinical trials are needed to provide more conclusive evidence for the future use of Salvia miltiorrhiza injection.
1‐O‐Hexyl‐2,3,5‐trimethylhydroquinone (HTHQ), a lipophilic phenolic agent, has an antioxidant activity and reactive oxygen species (ROS) scavenging property. However, the role of HTHQ on cerebral ischaemic/reperfusion (I/R) injury and the underlying mechanisms remain poorly understood. In the present study, we demonstrated that HTHQ treatment ameliorated cerebral I/R injury in vivo, as demonstrated by the decreased infarct volume ration, neurological deficits, oxidative stress and neuronal apoptosis. HTHQ treatment increased the levels of nuclear factor erythroid 2–related factor 2 (Nrf2) and its downstream antioxidant protein, haeme oxygenase‐1 (HO‐1). In addition, HTHQ treatment decreases oxidative stress and neuronal apoptosis of PC12 cells following hypoxia and reperfusion (H/R) in vitro. Moreover, we provided evidence that PC12 cells were more vulnerable to H/R‐induced oxidative stress after si‐Nrf2 transfection, and the HTHQ‐mediated protection was lost in PC12 cells transfected with siNrf2. In conclusion, these results suggested that HTHQ possesses neuroprotective effects against oxidative stress and apoptosis after cerebral I/R injury via activation of the Nrf2/HO‐1 pathway.
Stroke has become a major cause of death and disability worldwide. The cellular recycling pathway autophagy has been implicated in ischemia-induced neuronal changes, but whether autophagy plays a beneficial or detrimental role is controversial. Hydroxysafflor Yellow A (HSYA), a popular herbal medicine, is an extract of Carthamus tinctorius and is used to treat ischemic stroke (IS) in China. HSYA has been shown to prevent cardiovascular and cerebral ischemia/reperfusion injury in animal models. However, the specific active ingredients and molecular mechanisms of HSYA in IS remain unclear. Here, we investigated the effect of HSYA treatment on autophagy in a rat model of IS. IS was induced in rats by middle cerebral artery occlusion. Rats were treated once daily for 3 days with saline, HYSA, or the neuroprotective agent Edaravone. Neurobehavioral testing was performed on days 1, 2, and 3 post-surgery. Brains were removed on day 3 post-surgery for histological evaluation of infarct area, morphology, and for qRT-PCR and western blot analysis of the expression of the autophagy factor LC3 and the signaling molecules HIF-1[Formula: see text], BNIP3, and Notch1. Molecular docking studies were performed in silico to predict potential interactions between HSYA and LC3, HIF-1[Formula: see text], BNIP3, and Notch1 proteins. The result showed that HSYA treatment markedly alleviated IS-induced neurobehavioral deficits and reduced brain infarct area and tissue damage. HSYA also significantly reduced hippocampal expression levels of LC3, HIF-1[Formula: see text], BNIP3, and Notch1. The beneficial effect of HSYA was generally superior to that of Edaravone. Molecular modeling suggested that HSYA may bind strongly to HIF-1[Formula: see text], BNIP3, and Notch1 but weakly to LC3. In conclusion, HSYA inhibits post-IS autophagy induction in the brain, possibly by suppressing HIF-1[Formula: see text], BNIP3 and Notch1. HSYA may have utility as a post-IS neuroprotective agent.
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