ABSTRACT
Autophagy is a lysosome-dependent intracellular degradation process，and it is a key mechanism of diabetic cardiomyopathy （DCM）. Autophagy has dual regulatory effects on DCM. Under physiological conditions，normal autophagy can promote the decomposition of damaged cardiomyocytes and metabolites，so as to reduce the damage of harmful substances to the body and provide energy for cardiomyocytes. Under pathological conditions，the inhibited autophagy of cardiomyocytes will cause the accumulation of damaged cells and metabolites，which will cause damage to cardiomyocytes and eventually aggravate cardiac dysfunction in the patients with DCM. However，the over autophagy of cardiomyocytes will lead to autophagic death of a large number of cardiomyocytes and result in pathological myocardial remodeling and cardiac dysfunction，thus promoting the progression of DCM. Therefore，the restoration of a normal autophagy level is the key means to protect cardiomyocytes and improve the prognosis of DCM. Chinese medicine can regulate autophagy to treat DCM. Specifically，it can promote autophagy （making up for deficiency） or inhibit autophagy （removing excess） to restore the balance of autophagy，thereby alleviating DCM.
ABSTRACT
Bipolar disorder （BD） is considered to be mainly related to qi， phlegm， fire and deficiency. Binding constraint of liver qi is the initial cause， while phlegm and qi interact obstruction as well as phlegm and fire interact binding is the key pathogenesis of the transformation between depression and mania， and deficiency of both qi and yin is the main reason of the protracted course of disease. In clinical practice， BD is divided into binding constraint of liver qi pattern， phlegm and qi interact obstruction pattern， phlegm and fire interact binding pattern， and deficiency of both qi and yin pattern， which can be treated with Jinyu Shugan Powder （金玉疏肝散）， Kaiyu Wendan Decoction （开郁温胆汤）， Qingxin Huatan Decoction （清心化痰汤）， and Baihe Shengmai Beverage （百合生脉饮） in their modifications respectively； moreover， Guanye Jinsitao （Herba Hyperici Perforati） is usually used to rectify qi， relieve phlegm and clear heat. It is also suggested to put focus on the prevention and treatment of qi， phlegm and heat simultaneously， and modify the medicinals flexibly in accordance with the pathogenesis evolution and the abnormal exuberance.
ABSTRACT
AIM: To investigate t h e impacts of theaflavins (TFs) on neuronal apoptosis and blood-brain barrier (BBB) by regulating the calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2)/5 '-adenosine monophosphate-activated protein kinase (AMPK) signaling pathway. METHODS: Ninety rats were randomly separated into sham operation group, model group, low-dose TFs group (20 mg/kg TFs), high-dose TFs group (40 mg/kg TFs), and high-dose TFs + STO-609 group (40 mg/kg TFs + 10 ΜL CaMKK2 inhibitor-STO-609), positive control group (2 mg/kg nimodipine injection), with 15 rats in each group. A rat model of intracerebral hemorrhage was induced by collagenase type VII. The behavior of rats and the water content of brain tissue were detected; the serum of rats was isolated, and the levels of inflammatory factors-vascular cell adhesion molecule-1 (VCAM-1), tumor necrosis factor-α (TNF-α), and intercellular adhesion molecule-1 (ICAM-1) were detected; brain tissue around the hematoma was collected to detect neuronal apoptosis, BBB permeability parameter-EB level, and expressions of p-CaMKK2/CaMKK2, p-AMPK/AMPK and apoptosis-related protein Bax. RESULTS: Compared with the sham operation group, the mNSS score, ICAM-1, TNF-α, VCAM-1, brain tissue water content, apoptosis rate, EB level and Bax protein expression in the model group were all increased, both pCaMKK2/CaMKK2 and p-AMPK/AMPK were decreased (P < 0.05); compared with the model group, the mNSS score, ICAM-1, TNF-α, VCAM-1, brain water content, apoptosis rate, EB level and Bax expression in the low- and high-dose TFs groups and the positive control group were all lower than those in the model group, both pCaMKK2/CaMKK2 and p-AMPK/AMPK were increased (P < 0.05); compared with the high-dose TFs group, the mNSS score, ICAM-1, TNF-α, VCAM-1, brain tissue water content, apoptosis rate, EB level and Bax expression were all increased in the high dose TFs + STO-609 group, both p-CaMKK2/CaMKK2 and p-AMPK/AMPK were decreased (P < 0.05). CONCLUSION: TFs can reduce neuronal apoptosis, inflammatory response, BBB permeability, and play a protective role in rats with cerebral hemorrhage injury. Its mechanism is related to the activation of CaMKK2/AMPK signaling pathway.