Obesity is associated with numerous diseases and a shortened life expectancy ^[1]. Fat production is the maturation of fat cells by which preadipocytes become adipocytes, so they play an essential part in obesity ^[2]. In the process, 肥胖与许多疾病和预期寿命缩短有关[15]。脂肪产生是脂肪细胞的成熟，前脂肪细胞通过脂肪细胞成为脂肪细胞，因此它们在肥胖中起着重要作用[16]。在此过程中，CCAAT/enhancer-binding增强子结合蛋白 protein (C/EBP) and peroxisome proliferator-activated receptor γ (PPARγ) are thought to be the vital early regulatory proteins for lipogenesis. Adiponectin, sterol regulatory element-binding protein 1 (（C/EBP） 和过氧化物酶体增殖物激活受体γ （PPARγ） 被认为是脂肪生成的重要早期调节蛋白。脂联素、甾醇调节元件结合蛋白1（SREBP1), and fatty acid synthetase (FAS) are in charge of the production of mature fat cells ^[3]. ）和脂肪酸合成酶（FAS）负责成熟脂肪细胞的产生[17]。OA could inhibit the expression of the visceral fat-specific adipokine and downregulate 可以抑制内脏脂肪特异性脂肪因子的表达，下调PPARγ and 和C/EBPα to reduce the intracellular accumulation of fat in adipocytes ^[4]. Furthermore, ，减少脂肪细胞中脂肪的细胞内堆积[18]。此外，OA may reduce obesity via the suppression of the adipogenic factors 可以通过抑制成脂因子PPARα, 、SREBP1, and FAS ^[5]. 和FAS来减少肥胖[19]。OA has been shown to reduce the synthesis of fat and accelerate the utilization of fat through the alteration of hepatic 已被证明通过改变肝脏PPARα, recombinant carnitine palmitoyltransferase 1A (CPT1A), 、重组肉碱棕榈酰转移酶1A（CPT1A）、SREBP-1, the acetyl coenzyme A carboxylase, and coupled protein 1 (UCP1) ^[6]. In addition, 、乙酰辅酶A羧化酶和偶联蛋白1（UCP1）来减少脂肪的合成并加速脂肪的利用[20]。此外，OA can reduce blood glucose and lipid levels by promoting carbohydrate and fat metabolism ^[7]. Another piece of research showed that 可以通过促进碳水化合物和脂肪代谢来降低血糖和血脂水平[21]。另一项研究表明，OA can be effective against postmenopausal obesity by inhibiting fat synthesis acetyl-Co可以通过抑制脂肪合成乙酰辅酶A carboxylase (ACC) and upregulating essential genes for estrogen production, CYP11, CYP1, and 羧化酶（ACC）和上调雌激素产生的关键基因CYP11、CYP1和CYP17A19 ^[8].来有效对抗绝经后肥胖[22]。

Inflammation is crucial in obesity ^[9]炎症在肥胖中至关重要[23]; chronic inflammation in adipose tissue is primarily driven by macrophages ^[10] that are classified into two types: 脂肪组织中的慢性炎症主要由巨噬细胞驱动[24]，巨噬细胞分为两种类型：M1-type macrophages and 型巨噬细胞和M2-type macrophages ^[11]. An increase in the ratio of 型巨噬细胞[25]。M1/M2-type macrophages can enhance adipocyte growth, fat storage, and adipocyte differentiation ^[12]. Recent research has discovered that 型巨噬细胞比例的增加可以促进脂肪细胞生长、脂肪储存和脂肪细胞分化[26]。最近的研究发现，OA was able to reduce inflammation via the inhibition of macrophage infiltration, the 能够通过抑制巨噬细胞浸润、脂肪组织中的M1/M2 ratio in adipose tissues, reactive oxygen species (ROS), and decreasing NACHT, LRR, and PYD structural domain protein 3 (NLRP3) ^[13].比值、活性氧（ROS）以及降低NACHT、LRR和PYD结构域蛋白3（NLRP3）来减少炎症[27]。

Resistin is an adipocyte-specific secreted factor associated with adipocyte differentiation ^[14]. 抵抗蛋白是一种与脂肪细胞分化相关的脂肪细胞特异性分泌因子[28]。OA could reduce resistin synthesis in vivo by stimulating the cellular signaling transcriptional repressor three signaling and interfering with the tyrosine kinase 可以通过刺激细胞信号转导转录阻遏蛋白3信号转导和干扰酪氨酸激酶2-transcriptional signaling sensor activator ^[15]. Furthermore, glucose homeostasis and adipocyte differentiation are regulated by transcription factor hepatocyte nuclear factor 转录信号传导传感器激活因子来减少体内抵抗素合成[29]。此外，葡萄糖稳态和脂肪细胞分化受转录因子肝细胞核因子1b (（HNF1b) ^[16]. The research showed that ）的调节[30]。研究表明，OA could relieve glucose/lipid metabolic dysfunction via 可以通过HNF1b ^[17].缓解葡萄糖/脂质代谢功能障碍[31]。

The causes of obesity are complex, the symptoms are diverse, and multiple organs are implicated, so 肥胖的病因复杂，症状多样，涉及多个器官，因此OA in treating obesity is far from sufficient, especially in molecular mechanisms where it is even more insufficient. Therefore, more research is needed to demonstrate the role of OA in treating obesity.治疗肥胖还远远不够，尤其是在分子机制上更是不够的。因此，需要更多的研究来证明OA在治疗肥胖症中的作用。

Hyperlipidemia is defined as elevations of the fasting total cholesterol concentration, which could directly cause some severe diseases ^[18]. Numerous studies have suggested that 高脂血症定义为空腹总胆固醇浓度升高，可直接导致一些严重疾病[32]。大量研究表明，OA is beneficial in the treatment of hyperlipidemia. 对治疗高脂血症有益。OA could attenuate the triglycerides (TG) in rats by reducing the fat synthesis factor sterol regulatory element and activating transcription factor 1 ^[19]. 可以通过降低脂肪合成因子甾醇调节元件和激活转录因子1来减弱大鼠的甘油三酯（TG）[33]。OA also reduces total cholesterol (还通过抑制胆固醇酰基转移酶活性来减少总胆固醇（TC) formation by inhibiting cholesterol acyltransferase activity ^[20]. A high-fat diet will increase the level of peroxisome proliferator-activated receptor gamma coactivator ）的形成[34]。高脂肪饮食会增加过氧化物酶体增殖物激活受体γ共激活因子1β (（PGC-1β) leading to lipogenesis and very-low-density lipoprotein secretion ^[21]）的水平，导致脂肪生成和极低密度的脂蛋白分泌[35]; OA could decrease serum lipids in mice via the inhibition of 可通过抑制PGC-1β expression ^[22]. Clinical investigations also have shown that 表达降低小鼠的血脂[36]。临床研究还表明，OA decreased serum lipids in hyperlipidemic patients ^[23].可降低高脂血症患者的血脂[37]。

Hyperlipidemia is frequently one of the risk factors for various issues. Thus, improving blood lipids is critical for human health. Recent research demonstrated that 高脂血症通常是各种问题的危险因素之一。因此，改善血脂对人类健康至关重要。最近的研究表明，OA can decrease low-density lipoprotein-cholesterol (LDL-c), TC, and TG in mice. The process is thought to be connected to essential targets of lipid synthesis and accumulation.可以降低小鼠的低密度脂蛋白胆固醇 （LDL-c）、TC 和 TG。该过程被认为与脂质合成和积累的基本靶标有关。

高血压是心血管危险因素之一[38]。研究表明，One of the cardiovascular risk factors is hypertension ^[24]. Research revealed that OA was helpful in hypertension ^[25][26]. 对高血压有帮助[39,40]。OA could diminish vascular resistance by promoting nitric oxide (可以通过促进一氧化氮（NO) and inhibiting COX levels in isolated rat vessels ^[27]. ）和抑制离体大鼠血管中的COX水平来降低血管阻力[41]。OA also prevented hypertension in rats via the suppression of 还通过抑制NO catabolism ^[28]. Another study indicated that 分解代谢来预防大鼠高血压[42]。另一项研究表明，OA can improv可以通过增加e high blood pressure by increasing the expression of eNOS ^[29]. Meanwhile, NOS的表达来改善高血压[43]。同时，OA increased the vasodilator endothelium-derived hyperpolarizing factor (增加血管扩张剂内皮衍生的超极化因子（EDHF) and NO to maintain normal blood pressure ^[30].）和NO，以维持正常血压[44]。

The renin–肾素-血管紧张素系统和心房利钠肽（angiotensin system and attrial natriuretic peptide (ANP) are crucial to blood pressure homeostasis ^[31]. It was found that ， ANP）对血压稳态至关重要[45]。研究发现，OA can maintain the homeostasis of blood pressure by inhibiting the renin–angiotensin system and enhancing the fluid balance ^[32]. 可以通过抑制肾素-血管紧张素系统和增强体液平衡来维持血压的稳态[46]。OA also could increase the expression of atrial 还可以增加心房ANP, thus enhancing vascular homeostasis ^[33]. In addition, the diuretic and nephroprotective properties of 的表达，从而增强血管稳态[47]。此外，OA could reduce hypertension ^[34]. Furthermore, 的利尿和肾脏保护特性可以降低高血压[48]。此外，OA could improve hypertension via upregulating the anti-oxidative stress capacity and enhancing diuretic and natriuretic functions in hypertensive rats ^[35].可以通过上调高血压大鼠的抗氧化应激能力和增强利尿和利钠功能来改善高血压[49]。

Hypertension is one of the most prevalent systemic metabolic disorders ^[36]高血压是最普遍的全身性代谢紊乱之一[50]; hypertensive patients also have substantially elevated levels of lipid metabolites ^[37]. Numerous studies have demonstrated that reducing lipids can improve hypertension. 高血压患者的脂质代谢物水平也显著升高[51]。大量研究表明，降低血脂可以改善高血压。研究发现，OA was found to reduce hypertension by downregulating the expression of pro-inflammatory factor-secreting phospholipase 通过下调促炎因子分泌磷脂酶A2 and fat synthesis factor FAS and inhibiting lipid accumulation ^[38].和脂肪合成因子FAS的表达并抑制脂质积累来降低高血压[52]。

In conclusion, the incidence of hypertension has been rising steadily over the past decade, and the effective treatment of hypertension has a positive impact on middle-age and old-age patients. 综上所述，高血压发病率在过去十年中稳步上升，高血压的有效治疗对中老年患者具有积极作用。OA, a natural compound, can protect vascular endothelial cells, enhance body fluid balance, and promote glucose and lipid metabolism to reduce hypertension.是一种天然化合物，可以保护血管内皮细胞，增强体液平衡，促进葡萄糖和脂质代谢，从而降低高血压。

Non-alcoholic fatty liver is caused by hepatic steatosis in the liver ^[39]. Among the pathological mechanisms, the fat overloading in the liver triggered an inflammatory cascade response and subsequently developed into steatohepatitis ^[40]. Recent research indicated that 非酒精性脂肪肝是由肝脏脂肪变性引起的[53]。在病理机制中，肝脏中的脂肪超载引发了炎症级联反应，随后发展为脂肪性肝炎[54]。最近的研究表明，OA could delay the development of a nonalcoholic fatty liver by reducing inflammation, steatosis, and fibrosis in rats ^[41]. Furthermore, the liver could be in danger from microbial disorders and increased intestinal permeability, which may exacerbate the inflammatory responses to the nonalcoholic fatty liver ^[42]可以通过减少大鼠的炎症、脂肪变性和纤维化来延缓非酒精性脂肪肝的发育[55]。此外，肝脏可能面临微生物疾病和肠道通透性增加的危险，这可能会加剧对非酒精性脂肪肝的炎症反应[56]; research has shown that 研究表明，OA could treat nonalcoholic fatty liver by ameliorating intestinal barrier dysfunction and the Toll-like receptor 4 (TLR4)-associated inflammatory responses ^[43].可以通过改善肠道屏障功能障碍和Toll样受体4（TLR4）相关的炎症反应来治疗非酒精性脂肪肝[57]。

肝脂质超负荷诱导的氧化应激会加重肝损伤[58]。研究发现，Oxidative stress induced by a hepatic lipid overload exacerbates liver injury ^[44]. It was discovered that OA could substantially mitigate a nonalcoholic fatty liver by ameliorating hepatic oxidative stress and decreasing lipid synthesis factor 可以通过改善肝脏氧化应激和降低脂质合成因子SREBP1 ^[45].来显著减轻非酒精性脂肪肝[59]。

肝脏X受体（Liver X receptors (LXR) are highly expressed in the liver and responsible for cholesterol metabolism and homeostasis ^[46]， LXR）在肝脏中高度表达，负责胆固醇代谢和稳态[60]; LXR primarily activates the hepatic fat synthesis pathway by activating the promoter region of 主要通过激活SREBP-1 ^[47]. Research demonstrated that 的启动子区域来激活肝脏脂肪合成途径[61]。研究表明，OA was able to improve the abnormal accumulation of fat in the liver by reducing the expression of 能够通过降低LXR and the activity of 的表达和SREBP-1, as well as increasing the expression of reverse cholesterol transport (RCT)-related genes, including ATP-binding cassette transporter protein (ABC)A1 and ABCG1 ^[48]. Furthermore, 的活性，以及增加反胆固醇转运（RCT）相关基因的表达，包括ATP结合盒转运蛋白（ABC）A1和ABCG1，来改善肝脏中脂肪的异常堆积[62]。此外，OA could directly inhibit the expression of the 可直接抑制SREBP-1 protein and decrease fatty acid accumulation in the body, thus ameliorating the progress of nonalcoholic fatty liver ^[49].蛋白的表达，减少体内脂肪酸积累，从而改善非酒精性脂肪肝的进展[63]。

Briefly speaking, 简而言之，OA inhibits fat accumulation, accelerates cholesterol transport in the liver, and suppresses hepatic inflammation and oxidative stress in the treatment of nonalcoholic fatty liver.在治疗非酒精性脂肪肝时抑制脂肪堆积，加速胆固醇在肝脏中的转运，抑制肝脏炎症和氧化应激。

Diabetes mellitus is a metabolic disorder characterized by elevated blood sugar, mainly caused by an absolute or relative insulin deficiency and insulin resistance, classified as type 糖尿病是一种以血糖升高为特征的代谢性疾病，主要由绝对或相对胰岛素缺乏和胰岛素抵抗引起，分为1 and type 2, with type 2 comprising nearly 95% of cases ^[50]. Insulin sensitivity can be affected by oxidative stress, inflammation, and metabolic disorders.型和2型，其中近95%为2型[64]。胰岛素敏感性可能受到氧化应激、炎症和代谢紊乱的影响。

Inflammation is significant in diabetes mellitus ^[51]炎症在糖尿病患者中显著[65]; an inordinate increase of inflammatory factors hinders insulin receptor signaling and leads to insulin resistance ^[52]. Research has shown that the expression of 炎症因子的过度增加会阻碍胰岛素受体信号转导并导致胰岛素抵抗[66]。研究表明，OA可降低糖尿病大鼠TLR4, 、TLR9, interleukin 6 (IL-6), IL-18, tumor necrosis factor α (TNF-α), TNF-1, and C-reactive protein (CRP) was reduced by 、白细胞介素6（IL-6）、IL-18、肿瘤坏死因子α（TNF-α）、TNF-1和C反应蛋白（CRP）的表达[67,68,69,70]。此外，OA in diabetic rats ^{[53][54][55][56]}. Furthermore, OA also could improve insulin resistance by inhibiting the activity of nuclear factor还可以通过抑制核因子-κB (（NF-κB) ^[57].）的活性来改善胰岛素抵抗[71]。

氧化应激与糖尿病密切相关，并导致糖尿病的有害后果[72]。Oxidative stress is closely associated with diabetes and causes deleterious consequences of diabetes ^[58]. OA could improve the antioxidant capacity in diabetic rats by attenuating the levels of 可以通过降低NO and malonaldehyde (MDA), as well as enhancing the level of catalase (CAT) and superoxide dismutase (SOD) ^[59][60]. In addition, 和丙二醛（MDA）水平，以及提高过氧化氢酶（CAT）和超氧化物歧化酶（SOD）水平来提高糖尿病大鼠的抗氧化能力[73,74]。此外，OA was able to enhance the antioxidant function of mitochondria by increasing the expression of glutathione peroxidase 能够通过增加谷胱甘肽过氧化物酶4 (Gpx4) and SOD ^[61]. Furthermore, （Gpx4）和SOD的表达来增强线粒体的抗氧化功能[75]。此外，据报道，OA was reported to improve the mitochondrial ultrastructure and function and antioxidant capacity by inhibiting 通过抑制糖尿病大鼠的MDA and ROS levels, as well as increasing CAT, SOD, and glutathione peroxidase (和ROS水平以及增加CAT、SOD和谷胱甘肽过氧化物酶（GSH-px) in diabetic rats ^[62][63][64].）来改善线粒体超微结构和功能以及抗氧化能力[11,76,77]。

Diabetes is associated with disorders of energy metabolism ^[65]. Lipid accumulation and the dysregulation of glucose homeostasis are significant causes of insulin resistance ^[66]. It was demonstrated that 糖尿病与能量代谢紊乱有关[78]。脂质积累和葡萄糖稳态失调是胰岛素抵抗的重要原因[79]。研究表明，OA could improve diabetes by inhibiting the level of 可以通过抑制α-glucosidase and α-amylase ^[67]. Meanwhile, 葡萄糖苷酶和α-淀粉酶的水平来改善糖尿病[80]。同时，OA was able to improve diabetes in rats by stimulating insulin secretion ^[68] and decreasing blood glucose and blood lipid levels ^[69], increasing hepatic glycogen and muscle glycogen ^[70]. The research indicated that 通过刺激胰岛素分泌[81]、降低血糖和血脂水平[82]、增加肝糖原和肌糖原[83]来改善大鼠糖尿病。研究表明，OA could prevent hyper可以通过抑制葡萄糖吸收和促进葡萄糖向糖原的转变来预防高血糖[84]。血糖和糖化血红蛋白（glycemia by inhibiting glucose absorption and promoting the change of glucose to glycogen ^[71]. Elevated blood glucose and glycated heted hemoglobin， (HbA1c) levels (referred to as the prediabetic condition) occurred before the transition from normal to diabetic ^[72] and HbA1c）水平升高（称为糖尿病前期）发生在从正常到糖尿病的转变之前[85]，OA could improve glucose homeostasis via the reduction of blood glucose and 可以通过降低血糖和HbA1c levels ^[73]. It was verified that 水平来改善血糖稳态[86]。经证实，OA affects diabetes, which was related to increasin影响糖尿病，这与葡萄糖转运蛋白-5（g glucose transporter-5 (， GLUT-5) and ）和GLUT-4 expressions and decreasing FAS and ACC-1 expressions ^[74]. In addition, 表达增加以及FAS和ACC-1表达降低有关[87]。此外，观察到OA was observed to maintain glucose homeostasis in rats by decreasing the activity of hexokinase, the expression of glycogen phosphorylase (通过降低己糖激酶的活性、糖原磷酸化酶（GP), and increasing the expression of glycogen synthase (GS) ^[75]. Another study indicated that ）的表达和增加糖原合酶（GS）的表达来维持大鼠的葡萄糖稳态[88]。另一项研究表明，OA could accelerate glucose and lipid metabolism via increasing the level of 可以通过增加PPARγ/α and its related regulators, as well as 及其相关调节因子以及GLUT-4 and 和脂肪酸转运蛋白-1（fatty acid transport protein-1 (， FATP-1) proteins ^[76]. Furthermore, takeda ）蛋白的水平来加速葡萄糖和脂质代谢[89]。此外，武田G protein-coupled receptor 蛋白偶联受体5 (TGR5) belongs to the g-protein-coupled receptors involved in various cellular physiological effects ^[77]. By activating the expression of （TGR5）属于参与各种细胞生理效应的G蛋白偶联受体[90]。通过激活TGR5, 的表达，OA was able to decrease the blood glucose levels ^[78]. Based on the accumulated evidence, the imbalance of the phosphatidylinositol能够降低血糖水平[91]。根据积累的证据，磷脂酰肌醇-3-kinase (激酶（PI3K)/p）/蛋白激酶B（Protein kinase B (Akt) signaling pathway could cause the development of diabetes mellitus ^[79]. ， Akt）信号通路的不平衡可能导致糖尿病的发生[92]。经证实，OA was verified to inhibit gluconeogenesis by reducing the level of 通过降低Akt, forkhead box O1 (FoxO1), and glucose-6-phosphatase (、叉头盒O1（FoxO1）和葡萄糖-6-磷酸酶（G6Pase) ^[80]. It also exhibited that ）的水平来抑制糖异生[93]。该研究还表明，OA was able to accelerate glucose trans能够通过增加port by increasing p-Akt levels and GS levels, as well as decreasing GP levels ^[81][82]. Furthermore, -Akt水平和GS水平以及降低GP水平来加速葡萄糖转运[94,95]。此外，OA has positive effects on diabetes via increasing 通过增加PI3K/Akt and AMPK 和AMPK磷酸化、磷酸烯醇丙酮酸羧激酶（phosphorylation, phosphoenolpyruvate carboxykinase (PEPCK), and ， PEPCK）和G6Pase levels, as well as decreasing the level of the mammalian target of rapamycin (mTOR) ^[83]. It was discovered that 水平以及降低哺乳动物雷帕霉素靶标（mTOR）水平，对糖尿病有积极作用[96]。研究发现，OA could improve insulin resistance through the activation of the level of the insulin receptor substrate (可以通过激活胰岛素受体底物（IRS-1) and ）和PI3K/Akt ^[84]. Moreover, 的水平来改善胰岛素抵抗[97]。此外，OA may normalize insulin, 可使胰岛素、高密度脂蛋白（high-density lipoprotein (HDL), IRS1, GLUT2, GLUT4, and Akt levels, and decrease TC, TG, and low-， HDL）、IRS1、GLUT2、GLUT4和Akt水平正常化，并降低TC、TG和低密度脂蛋白（lowdensity lipoprotein (LDL) levels ^[85]. Furthermore, ， LDL）水平[98]。此外，OA could decrease insulin resistance by improving 可以通过改善β-cells ^[86].细胞来降低胰岛素抵抗[99]。

High-glucose environments have been found to cause endothelial cell dysfunction ^[87][100]. Research has shown that OA attenuated human umbilical vein endothelial cells (HUVECs) function damage via activating PPARδ, increasing the phosphorylation of Akt and eNOS ^[88][101]. Furthermore, persistent hyperglycemia will change blood composition, such as erythrocyte morphology ^[89][102], and increase the production of erythropoietin (EPO) ^[90][103]. OA could improve diabetes by reducing plasma glucose, HbA1c, and EPO levels and increasing the antioxidant capacity of erythrocytes ^[91][104].

Complications caused by diabetes are also a leading cause of harm to human health, such as diabetic nephropathy ^[92][105]. Research reported that OA could protect rats against diabetic nephropathy by restoring plasma aldosterone and renal injury molecule-1 ^[93][106]. In addition, advanced glycosylation end products, such as renal N-(carboxymethyl) lysine, HbA1c, and glycosylated albumin, are also related to the development of diabetic nephropathy ^[94][107]. OA was able to inhibit diabetic nephropathy via a reduction of the level of renal N-(carboxymethyl) lysine, HbA1c, urinary albumin, and urine glycated albumin, as well as increasing the level of plasma insulin and renal creatinine clearance ^[95][108]. Furthermore, OA could also restore the damaged renal structure by increasing insulin secretion, renal units, and endothelial-selective adhesion molecules, and decreasing urinary albumin/creatinine levels ^[96][109].

There is accumulating evidence that OA cures diabetes by decreasing inflammation, reducing oxidative stress, and protecting endothelial cell function. Furthermore, OA could enhance the glucose–lipid metabolism in diabetic rats, restore blood components damaged by high glucose levels, and alleviate diabetic nephropathy problems. To summarize, OA in the treatment of diabetes mellitus has shown tremendous potential and is supported by numerous pieces of research; however, this research may require additional clinical trials to confirm. The detailed pharmacological effects of OA on metabolic syndrome are shown in Table 1. 

is considered a ligand-activated transcription factor that regulates the glycolipid metabolism, and adiponectin promotes fatty acid biosynthesis and inhibits hepatic gluconeogenesis ^[124]. 被认为是一种配体激活的转录因子，可调节糖脂代谢，脂联素可促进脂肪酸生物合成并抑制肝脏糖异生[136]。OA could reduce lipids and enhance high-density lipoprotein cholesterol (HDL-c) by increasing 可以通过增加PPARγ and adiponectin Receptor 1 (和脂联素受体1（AdipoR1) Levels, decreasing ）水平来降低脂质并增强高密度脂蛋白胆固醇（HDL-c），从而降低AdopoR2 levels ^[125].水平[137]。

Farnesoid-X-receptor， (FXR) is associated with the bile metabolism ^[126], and angiotensinFXR与胆汁代谢有关[138]，血管紧张素1-7 (（Ang1-7) has been implicated as an AS protector ^[127]. ）被认为是AS保护因子[139]。发现OA was found to decrease the levels of lipids in rats via the regulation of the expression of 通过调节FXR and 和Ang1-7 ^[128]. In addition, 的表达来降低大鼠的脂质水平[13]。此外，OA 抑制inhibited the expression of iNOS, thereby delaying the progression of aortic stenosis ^[129].NOS的表达，从而延缓主动脉瓣狭窄的进展[140]。

In conclusion, 综上所述，OA can reduce the area of vascular lipid plaque and treat AS by protecting 可以通过保护HUVECs, reducing inflammatory factors and the accumulation of lipids. The detailed pharmacological effects of OA on metabolic syndrome-related cardiovascular diseases are shown in Table 2.

Stroke is one of the main causes of increased mortality ^[97][110], which is affected by inflammation, oxidative stress, and nerve damage ^[98][111].

The key mechanism in the formation of ischemic stroke is oxidative stress ^[99][112], which also causes neuronal apoptosis, inflammation, and nerve injury ^[100][113]. It was reported that OA reduced cerebral ischemic stroke damage by increasing the level of mitochondrial antioxidant α-tocopherol (α-TOC) and GSH, as well as decreasing the leakage of the damage marker lactate dehydrogenase (LDH) ^[101][114]. Furthermore, OA was able to improve oxidative stress in brain-injured rats; the results showed that OA treatment significantly increased the activity of SOD, GSH-Px, mitochondrial membrane potential (MMP), and succinate dehydrogenase (SDH), and decreased MDA and LDH levels ^[102][115]. Meanwhile, OA also could restrain the blood–brain barrier indicator occludin, matrix metalloproteinase 9 (MMP9), and Evans blue leakage, and inhibit oxidative indicator dihydroethidium fluorescence and MDA expression ^[103][116]. In addition, heme oxygenase-1 (HO-1) is the most effective antioxidant response element, and glycogen synthase kinase-3β (GSK-3β) is able to regulate HO-1 in controlling oxidative stress ^[104][117]. OA attenuated cytotoxicity and ROS via the regulation of the GSK-3β/HO-1 signal in rats ^[105][118].

In general, 一般来说，天然产物来源的OA from natural product sources has neuroprotective functions, such as the improvement of the blood–brain barrier, reduction of nerve injury, and cerebral edema in mice; the mechanism was primarily associated with the improvement of oxidative damage. However, it remains to be determined whether OA in stroke treatment has a more promising mechanism.具有神经保护功能，如改善小鼠的血脑屏障、减少神经损伤和脑水肿;该机制主要与氧化损伤的改善有关。然而，脑卒中治疗中的OA是否具有更有希望的机制还有待确定。

Heart disease has a high mortality rate, and the number of deaths is still rising ^[106]. Oxidative stress is a significant reason for heart disease心脏病的死亡率很高，死亡人数仍在上升[119]。氧化应激是心脏病的重要原因; the elevated expression of ROS causes cardiomyocyte dysfunction and damage ^[107]. Research demonstrated that 表达升高会导致心肌细胞功能障碍和损伤[120]。研究表明，OA promoted the antioxidant capacity of the heart via the reduction level of the lipid peroxidation products ^[108]. Furthermore, 通过降低脂质过氧化产物的水平来促进心脏的抗氧化能力[121]。此外，OA was able to prevent diabetic cardiomyopathy through the regulation of 能够通过调节HO-1/Nrf2 to increase SOD and GS, as well as decrease MDA and GP ^[109]. Meanwhile, 来增加SOD和GS，并降低MDA和GP[122]。同时，OA was verified to prevent CVDs by improving the inflammatory reaction, 通过改善大鼠的炎症反应、MDA, SOD, GPx, as well as heart weight in rats ^[110]. In addition, 、SOD、GPx和心脏重量来预防CVDs[123]。此外，OA 可以通过增加抗氧化能力和降低细胞凋亡信号转导could improve myocardial apoptosis by increasing the antioxidant capacity and decreasing apoptosis signaling caspase-3 and BAX activity, increasing Bcl-2 activity ^[111][112].aspase-3和BAX活性，增加Bcl-2活性来改善心肌细胞凋亡[124,125]。

内皮素1（Endothelin 1 (ET-1) aggravates the development of CVDs ^[113], and ， ET-1）加重心血管疾病（CVDs）的发生[126]，OA could inhibit cardiomyocyte injury through the regulation of the expression of 可通过调节ET-1 ^[114]. Furthermore, 的表达来抑制心肌细胞损伤[12]。此外，ET-1 and 和NF-κB modulate the fibrotic process in the heart, as well as promote the expression of fibronectin in cardiac tissues ^[115]. 可调节心脏中的纤维化过程，并促进心脏组织中纤连蛋白的表达[127]。OA could improve fibrotic hearts in rats by reducing the activation of 可以通过减少NF-κB and ET-1 ^[116]. Moreover, the 和ET-1的激活来改善大鼠的纤维化心脏[128]。此外，Akt/mTOR exacerbates the pathological process of myocardial remodeling ^[117]加剧了心肌重塑的病理过程[129]; OA performed cardiac protection with the inhibition of vascular remodeling by decreasing the levels of Akt and mTOR ^[118]. In addition, 通过降低Akt和mTOR水平来抑制血管重塑，从而起到心脏保护作用[130]。此外，OA possessed the ability to suppress the platelet aggregation mediated by phospholipase 具有抑制磷脂酶C, thereby aiding in the prevention of cardiovascular thrombosis ^[119].介导的血小板聚集的能力，从而有助于预防心血管血栓形成[131]。

Therefore, current research demonstrates that 因此，目前的研究表明，OA could treat a variety of heart diseases, as well as prevent cardiac fibrosis and the cardiac remodeling process. The mechanism includes the inhibition of inflammation, oxidative stress, and the improvement of the expression of vasoconstrictive factors.可以治疗多种心脏病，以及预防心脏纤维化和心脏重塑过程。其机制包括抑制炎症、氧化应激和改善血管收缩因子的表达。

动脉粥样硬化（Atherosclerosis (AS) is the underlying pathology of CVDs ^[120]. a， AS）是CVD的潜在病理学[132]。OA could prevent 可以通过抑制氧化应激、内皮功能障碍和脂质沉积等多种病理发展来预防AS by inhibiting many pathological developments, such as oxidative stress, endothelial dysfunction, and lipid deposition. Oxidative stress was deemed the critical mechanism in AS ^[121]. Research demonstrated that 。氧化应激被认为是AS的关键机制[133]。研究表明，OA may safeguard HUVECs damage by inhibiting the leve可能通过抑制脂蛋白受体1（ls of lipoprotein receptor 1 (LOX-1), ROS, as well as hypoxia-inducible factor 1 α (， LOX-1）、ROS以及缺氧诱导因子1 α（HIF-1α) ^[122]. Moreover, OA has been confirmed to alleviate ）的水平来保护HUVECs damage via the reduction in the level of 损伤[134]。此外，OA已被证实可以通过降低ROS and 和LOX-1, as well as enhancing the level of 的水平以及提高Nrf2/HO-1 ^[123].的水平来减轻HUVECs的损害[135]。

PPARγ