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【Covid-19】Causes & mechanisms that promote thromboinflammation in COVID-19

My little understanding about the causes & mechanisms that promote thromboinflammation in COVID-19.

Contents:

1. How Covid-19 virus enters the human body?

2. What is the function of ACE2?

3. How SARS-CoV-2 virus lead to thromboinflammation?

    3a. Excessive ANG II

    3b. Elevated Levels of Tissue Factor (TF)

    3c. PAR Signaling

    3d. Formation of Neutrophil Extracellular Traps (NETs)

    3e. Purinergic signaling

4. Conclusion

5. References


1. How Covid-19 virus enters the human body?

Spike-like protein on the SARS-CoV-2 virus binds to Angiotensin-Converting Enzyme 2 (ACE2). Subsequently, the virus enters and starts replication, causing ACE2 to function abnormally.

SARS-CoV-2 virus binds to ACE2
SARS-CoV-2 virus binds to ACE2

2. What is the function of ACE2?

Normally, ACE2 protein help to modulate the activities of a protein called angiotensin II (ANG II). ACE2 will be in charge of converting ANG II to other molecules, mostly the ANG 1-7 which can counteract the effects of ANG II.

ANG II will increase blood pressure and inflammation by increasing damage to blood vessel linings and various types of tissue injury. Hence, ACE2 is essential to maintain the normal level of inflammation.

 

3. How SARS-CoV-2 virus lead to thromboinflammation?

3a. Excessive ANG II

As mentioned earlier, the SARS-CoV-2 virus bind to ACE2, cause ACE2 to function abnormally. Therefore, the ANG II signaling is no longer restricted by ACE2. So the ANG II will increase while the ANG 1-7 will decrease tremendously.

As a result, more ANG II is available to injure tissues and blood vessels that will lead to inflammation.

Increase of ANG II---increase inflammation
Increase of ANG II---increase inflammation

3b. Elevated Levels of Tissue Factor (TF)

Dysregulation in angiotensin II signaling induces the synthesis & expression of the cell surface glycoprotein tissue factor (TF) in various cell types.

Tissue factor (TF), is also known as platelet tissue factor, or Factor III. It acts as primary initiator of the extrinsic pathway in blood coagulation.

Coagulation Pathway
Coagulation Pathway

Along the extrinsic pathway, the tissue factor will cause the conversion of factor 7 to become activated factor 7.

Then, the tissue factor combines with the activated factor 7 and calcium ions to convert factor 10 into activated factor 10. 

The activated factor 10 will then, in the presence of calcium ions and factor 5, forms prothrombin activator.

And this prothrombin activator will cause the conversion of prothrombin, which is factor 2 into activated factor 2, which is also known as thrombin.

Thrombin is a clotting enzyme. The activated thrombin will act in two ways. 

The first one, thrombin further activates factor 1, which is known as fibrinogen. Thrombin link fibrinogen together, become fibrin. A lot of fibrin link together to become fibrin mesh.

Thrombin further activates fibrinogen
1. Thrombin further activates fibrinogen

The second way is thrombin activate factor 13, which is the fibrin stabling effect. Factor 13 will make crosslinking of fibrin. This fibrin mesh has high fiber density and increases resistance to fibrinolysis. Normally it holds the platelet plug in place. In this case, it becomes a thrombus, leading to thrombosis. 

Thrombin activate fibrin stabling effect
2. Thrombin activates fibrin stabling effect


Besides, tissue factor also can enter intrinsic pathway by releasing polyphosphates which are stored in platelet. Polyphosphates active factor 12. Activated factor 12 can contribute to inflammation by its activation of kallikrein, thereby increasing the formation of bradykinin, leading to inflammation reaction. 

Besides, kallikrein stimulates the activation of Factor 12, which enters the intrinsic pathway, leading to thrombosis. Thus, activation of coagulation by tissue factor can have multiple thromboinflammatory effects via the diverse effects of activated factor 12
activation of coagulation by tissue factor can have multiple thromboinflammatory
Activation of coagulation by tissue factor can have multiple thromboinflammatory

3c. PAR Signaling

Let refers back to the activation of thrombin.

Thrombin (factor 2) is activated by prothrombin, and further convert the soluble fibrinogen into insoluble fibrin at the wound. 

On the other hand, the thrombin will also activate the platelet through protease-activated receptor 1 ​(PAR1) on the platelet surface.

PAR1, which is the short form of protease-activated receptor 1, is actually a G protein-coupled receptor (GPCR).

The activation of PAR1 is accomplished when the thrombin binds to, and cleaves the N-terminal exodomain of PAR1 at a specific site. 

This cleavage generates a new receptor N terminus and thereby unmasks a “tethered ligand” that binds to PAR 1 receptor, as shown in the picture on the right. As a result, it causes the activation of platelets.

Activation of PAR1
Activation of PAR1

It is also noteworthy that just one molecule of thrombin can activate multiple PAR 1 receptors. 

Therefore, even a small amount of thrombin can activates a great amount of platelets, and further amplifies the coagulation cascade that results in more thrombin, more fibrin and more activated platelets. 

As a result, the clot will become larger and larger, until a thrombus occludes the blood flow through the blood vessels. 

3d. Formation of Neutrophil Extracellular Traps (NETs)

When there is tissue damage or lung damage in COVID-19 patients, the neutrophils, one of the white blood cell types will release cathelicidins to activate platelets.

And the activated platelet will react in two ways. 

Firstly, activated platelet will promote their adhesion to monocytes and neutrophils. This will lead to Neutrophil-platelet aggregation or Neutrophil extracellular traps (NETs). 

Secondly, the activated platelet will secrete proinflammatory factors (e.g., IL-1b,RANTES), prothrombotic entities (e.g., TXA2) and platelet-activating factor (PAF). 

Both actions, especially the NETS, will further enhance inflammation and platelet activation. 

Lastly, this thrombin-mediated activation of platelets will also result in the secretion of ADP, which further initiates purinergic signaling.


3e. Purinergic signaling

Purinergic signaling via ADP is a key mechanism for platelet activation. 

ADP can obtain from:
1. Extracellular ADP
2. ADP released by activated platelet (From dense granules)

ADP further bind with purinergic receptor P2Y12 and P2Y1, cause activation of purinergic receptor by exchanging GDP to GTP.

-P2Y12 belong to Gi class of GPCR---Inhibit cAMP pathway
-P2Y1 belong to Gq class of GPCR----IP3 Pathway

*Both Gi and Gq are the subunit of alpha

P2Y12 and P2Y1 pathway
P2Y12 and P2Y1 pathway


After activation, Gi Alpha subunit activated. It inhibits the Adenyl Cyclase which in turn deactivates the cAMP (cyclic Adenosine Monophosphate) pathway. Further inhibit Protein kinase A (PKA), Protein kinase A (PKA) promote the activation of Gp2b 3a complex, which is fibrinogen receptor. Let look at picture. When cell damage, it will secrete von Willebrand factor and cause formation platelet plug. To form a nice platelet plug, Gp2b 3a complex bind the platelet together via fibrinogen.

Gp2b 3a complex bind the platelet together via fibrinogen
Gp2b 3a complex bind the platelet together via fibrinogen


Next, the mechanism of P2Y1 receptor. activated Gq alpha subunit which drives the Phospholipase C (PLC) activation. Phospholipase C (PLC) break down specific membrane bound structure which called Phosphatidylinositol Biphosphate (PIP2). Phosphatidylinositol Biphosphate (PIP2) further break into two components, diacylglycerol (DAG) and Inositol triphosphate (IP3). diacylglycerol (DAG) activate Protein kinase C (PKC) which further activate Gp2b 3a complex, which is fibrinogen receptor. 

Phosphatidylinositol Biphosphate (PIP2) activates Inositol triphosphate (IP3) pathway which promote intracellular release of calcium, leading to platelet activation. Besides, Phospholipase C (PLC) activation also drives the granule secretion from platelets. Among the secretion, TXA2, ADP and PAF are responsible to platelet activation.

Moreover, Gi also can activate Gq, enhance platelet activation and platelet plug

4. Conclusion

The mechanisms that discuss earlier actually are positive feedback loop. 
Coronavirus 2 bind with ACE 2, result in decreases ACE 2 activity and ANG2 increase. ANG2 increase cell damage which further cause inflammation and platelet activation, either via PAR or purinergic signaling. ​Thus, platelet activation leads to coagulation and then certain secretion or formation will further enhance inflammation and platelet activation, such as thrombin, ADP, etc.​ 

Due to this positive loop, platelet plug keeps forming and ultimately cause thrombosis.

positive feedback loop
Due to this positive loop, platelet plug keeps forming and ultimately cause thrombosis.


5. References:

MEDSimplified. (2015, October 22). Coagulation cascade simplest explanation! The extrinsic and 
intrinsic pathway of Hemostasis. [Video]. Youtube. https://www.youtube.com/watch?v=LVYmV5mK6QI

Medmovie, (2017). PAR1 Inhibitors (Vorapaxar) Medmovie MOD/MOA Sample Only. [Video]. 
Youtube. https://www.youtube.com/watch?v=uYpv8T7Qoh0

Medicosis Perfectionalis. (2019). P2Y12 Receptor: Mechanism of Platelet Aggregation. [Video]. Youtube. 
https://www.youtube.com/watch?v=PzfirRCNMPU

Medicosis Perfectionalis. (2019). P2Y12 Receptor Inhibitors. [Video]. Youtube. 
https://www.youtube.com/watch?v=sw6gI5PqjM4

Medicosis Perfectionalis, (2019). GPIIb/IIIa receptor inhibitors. [Video]. Youtube.  
https://www.youtube.com/watch?v=YNxE6jSARog

Medicosis Perfectionalis. (2019, May 27). Protein C and Protein S. [Video]. 
Youtube. https://www.youtube.com/watch?v=aJ77PhXcVso

Medicosis Perfectionalis. (2020, August 15). Direct Thrombin Inhibitors and Factor Xa 
Inhibitors | Pharmacology |Hematology. [Video]. Youtube. https://www.youtube.com/watch?v=xQo7AZ3VQTQ

Ninja nerd lecture. (2017, March 18). Hematology | Hemostasis: Coagulation Cascade. [Video]. 
YouTube. https://www.youtube.com/watch?v=SGzp9wqeu84&feature=youtu.be%20%E2%80%8B

NCBI. (2010, November 23). What is inflammation? 
Retrieved from  https://www.ncbi.nlm.nih.gov/books/NBK279298/%E2%80%8B/%E2%80%8B/%E2%80%8B/

NCBI. (n.d.). Thrombosis. Retrieved from  
http://www.ncbi.nlm.nih.gov/mesh/68013927%E2%80%8B

Press Release. (2021, May 17). The Noble Assembly At The Karolinska ​Institute. 
Retrieved from https://www.nobelprize.org/prizes/medicine/1982/press-release/
Sriram, K., & Insel, P. A. (2021). Inflammation and thrombosis in COVID-19 pathophysiology: ​
Proteinase-activated and purinergic receptors as drivers and candidate therapeutic targets. Physiological Reviews, 101(2), 545-567. https://doi.org/10.1152/physrev.00035.2020​

The Conversation Media Group Ltd. (2020, May 14). What is the ACE2 receptor, how is it connected  
to coronavirus and why might it be key to treating COVID-19? The experts explain. Retrieved from https://theconversation.com/what-is-the-ace2-receptor-how-is-it-connected-to-coronavirus-and-why-might-it-be-key-to-treating-covid-19-the-experts-explain-136928# 


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【方剂学】 涩肠固脱剂--真人养脏汤(原名纯阳真人养脏汤)

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【Pharmacology & 方剂学】Traditional Chinese Medicine (TCM) – Does its contemporary business booming and globalization really reconfirm its medical efficacy & safety?

Traditional Chinese Medicine (TCM) – Does its contemporary business booming and globalization really reconfirm its medical efficacy & safety? 笔记 1. Introduction 有几个国家同意中医 Promoting the globalization of TCM, Traditional Chinese medicine has been spread to 183 countries and regions around the world.  According to the World Health Organization,  103 member states have given approvalto the practice of acupuncture and moxibustion 29 have enacted special statutes on traditional medicine 18 have included acupuncture and moxibustion treatment in their medical insurance provisions  2. What's in the TCM bottle? The philosophy behind Chinese medicine is a melding of tenets from Buddhism, Confucianism, and the combined religious and philosophical ideas of Taoism.  TCM is based on the concept that illness occurs when a person's “internal Qi” falls out of balance.  Qi: the word the Chinese use to describe the un-measurable energies that theoretically permeate ev...

【方剂学练习题】 各论:第一章 解表剂

【方剂学练习题】 各论:第一章 解表剂 一、填空题 1 .麻黄汤和大青龙汤中,麻黄和桂枝的配伍比例分别是 _______ 、 _______ 。             ANS: 3:2 ; 3:1       解析:麻黄汤:麻黄 9g ;桂枝 6g             大青龙汤 : 麻黄 12g ;桂枝 6g   2 .桂枝汤证和麻黄汤证的脉象分别是 ______ 、 ________ 。         ANS: 浮缓 ; 浮紧       解析:桂枝汤:外感风寒表虚证             麻黄汤:外感风寒表实证   3 .桑菊饮的功用是 _______ ,主治 _______ 。         ANS: 疏风清热 , 宣肺止咳;风温初起   4 .以组方原则论,败毒散中人参属于 ______ 药;参苏饮中人参属于 ________ 药。         ANS :佐 ; 佐   5 .被称为“四时发散之通剂”的方剂是 _______ ;被称为“辛凉轻剂”的方剂是 _______ 。         ANS: 九味羌活汤 ; 桑菊饮   6 .银翘散中,为助君药发散外邪,透邪外出而加入辛而微温的两味药分别是 _______ 、 _______ 。         ANS: 荆芥穗 ; 淡豆豉       解析:风温之邪居卫,恐惟用辛凉难开其表,遂入辛而微温之 ...

【TCM & Western Medicine】阿片类药物(Opioids)& 中药

阿片类药物(Opioids) 是治疗中重度疼痛的首选药物。 其不良反应主要包括: 便秘 恶心呕吐 瘙痒 头晕 尿潴留 嗜睡 谵妄 认知障碍 呼吸抑制 Related link:  【Pharmacology】OPIOIDS 内容: 1. 癌性疼痛 2. 便秘 3. 阿片类成瘾慢性稽延症状 4. 参考文献 1. 癌性疼痛 是晚期恶性肿瘤最常见症状之一 被列为“第五生命体征” 生命四大体征:呼吸、体温、脉搏、血压 癌痛治疗的药物: 非甾体类抗炎药物 (Non-Steroidal Anti-Inflammatory Drug) 阿片类药物 (Opioids) 中医 癌性疼痛属“痛证”范畴 病因:正气亏虚、邪毒内侵 病机:“毒、瘀”壅塞经络 治疗:行气活血、化瘀解毒功效的中药组方外敷联合西药治疗 好处: 增强止痛效果 缩短止痛起效时间 延长镇痛时间从而减少爆发痛次数 提高患者的生活质量 一定的抗肿瘤作用 中药方: “双黄散结散” 全方具有清热解毒、散结止痛的作用。 君: a. 大黄 (Rhubarb) 苦寒泻热:荡涤胸腹之邪热 b. 黄柏 (Phellodendron amurense Rupr) 苦寒泻热:清下焦热 & 大黄:清热解毒散结 臣: a. 苦参 (Sophora flavescens) b. 蒲公英 (Dandelion Herb) 加强清热解毒之功 c. 三棱 (rhizoma sparganii) d. 莪术 (Curcuma) 破血逐瘀 佐使: a. 乳香 (frankincense) 行气舒筋 b. 没药 (Myrrh) 行气化瘀 & 乳香:活血定痛 c. 冰片 (Borneol) 通窍散火、消肿止痛 **现代研究亦表明,大黄、黄柏、冰片、乳香、没药、三棱、莪术、蒲公英等药物均有有很好的抑制肿瘤、止痛等作用。 另外一方: 川芎、白芷、姜黄、乳香、没药、肿节风、山慈姑、蚤休、麻黄、白芥子、王不留行 11味中药精细加工成粉并与凡士林调和而成膏状 功能:扶正气、消肿痛、活血化瘀,调畅经脉,透皮达里,引诸药直达病所。 好处: 避免了异体蛋白过敏现象 因其主要成分为植物 避免药物通过肝脏时的首过效应 其中药有效成分透过皮肤屏障,直接进入人体循环,无胃肠降解和胃肠刺激作用 治疗疼痛效果明显、持续时间长 无不良反...

【Beauty 】面部刮痧

 面部刮痧 作用: 促进血液循环 消除脸部水肿 紧致肌肤 注意事项: 刮痧后2小时不要洗脸 刮痧之后毛孔处于打开的状态。去洗脸的话会让寒气进入身体 手法 先做左边,因为气机是左升右降,从左开始是调节阳气,因此不论哪种按摩建议都要从左到右。 步骤 1. 涂抹一些油,轻轻按压 2. 开穴 从左至右轻揉各个穴位,跟着上图所示由承浆穴开始开穴,最后以印堂穴做结尾。 3. 刮淋巴 耳后顺着颈部 4. 额部刮痧 5. 眼部刮痧 眉毛和眼眶 6. 面部刮痧 迎香穴到太阳穴刮3次。 地仓穴到耳门刮3次。 承浆穴到听会刮3次。 一手按住额前,并用刮痧版的凹面去刮下颌,重复3次。 对准法令纹并刮到耳前,最后从颈部排出去,重复3次。 从嘴角出发至颧骨下方,停留在苹果肌并将刮痧版转向, 接着刮到太阳穴并重复3次。 7.颈部刮痧 疑问 1. 为什么要从承奖开始? 从承浆开始,是为“引气开门”;以印堂结束,是为“收气归神”。 承浆穴 是 任脉 上的穴位,具有“开关”性质。 宣通任脉、疏通下行之气 任脉是“阴脉之海”,主一身之阴,从下往上走,承浆作为任脉收尾,是开启整条任脉的“水龙头”之一,先打开它,有利于整条经脉气血流通。 引气上行,排浊生清 面部刮痧会产生向上提升的作用,先开承浆可以把体内浊气引导下行,从而避免“气堵于上”,减轻面部沉滞。 承浆为“百穴之始” (在部分刮痧法中) 有些手法认为它是面部开穴的“起始点”,先开此穴,犹如开门迎气,后续效果更佳 印堂穴 属督脉,又称“上丹田”,具有安神、聚气、提升精神的作用。 收气归元,安神定心 刮痧结束后以印堂为收尾,有“收气”之意,帮助把整个疏通后的气血归于中心、稳定神志。 印堂属上焦门户,最后激活提神 这是面部的“神气之门”,最后刺激它,有种“提气、醒神”的效果,让整个面部状态归于清明。 符合气血运行的方向:下→上→中收 这种走向符合中医“先开下,后通上,最后归中”的思路,利于气血顺畅、面部轮廓向上提拉。 “我们从承浆开始,是为了先打开下面的任脉,把气血引出来,整个面部才会通畅;最后在印堂结束,帮助收气安神,效果更稳定。” 2. 为什么刮淋巴 促进代谢废物的排除;提升免疫力,减少炎症(痘痘);加快面部轮廓紧致;经络气血更顺畅,排湿气 促进体内“代谢废物”的排出 淋巴系统像“体内垃...