Table 1.

The treatment mechanism of MA in treating diseases of various organs are summarized.

Organs	In Vivo/In Vitro	Diseases	Treatment Mechanism	References
Brain
	In vivo	AD	MA promotes the expression of BDNF, reduces the apoptosis of neurons, improves the memory and cognitive impairment of mice caused by cholinergic system damage, and enhances the cognitive function of mice	[82]
	In vivo	Epilepsy	MA can reduce the production of inflammatory factors, reduce the level of glutamate in the hippocampus, improve the antioxidant capacity of the hippocampus and thus improve the production of epileptic behavior	[89]
	In vitro	Ischemic stroke	MA can block the cell necrosis induced by hypoxia, reduce the necrosis of neurons, effectively prevent the damage of cell bodies and neurites, and increase the survival rate of neurons	[90]
	In vivo	Ischemic stroke	MA prolonged the therapeutic time window of MK-801 from 1 h to 3 h. MA and MK-801 jointly increased the level of glutamate transporter GLT-1 in astrocytes and promoted astrocytes to regulate glutamate excitotoxicity, thus playing a therapeutic role in ischemia	[92]
	In vivo	Ischemic stroke	MA can significantly prevent axon injury, promote axon regeneration and increase the expression of synaptophysin after 7 days of ischemia	[93]
	In vivo	Ischemic stroke	MA treatment can enhance the expression of glial glutamate transporter GLT-1 at the protein and mRNA levels, leaving extracellular glutamate at a low concentration, thus playing a protective role in nerve cells during stroke ischemia	[91]
	In vitro	Astrocytoma (1321N1 cells)	MA can induce apoptosis of 1321N1 cell line	[77]
Lung
	In vitro	Lung cancer (A549 cells)	MA treatment mediates mitochondrial apoptosis pathway and HIF-1 α pathway induced apoptosis of A549 cells	[59]
	In vitro	Lung cancer (A549 cells)	MA can promote the expression of caspase-3, caspase-8 and caspase-9 by regulating the expression of Smac and reducing the expression of c-IAP1, c-IAP2, XIAP and survivin, thereby inducing apoptosis of A549 cells	[60]
	In vivo	Lung damage	MA antagonizes lung injury caused by diesel PM2.5 by regulating TLR4-MyD88 and mTOR autophagy pathway	[94]
	In vivo	Lung injury	MA exerts anti-inflammatory effects by down-regulating NF-κB and p-STAT-1 to regulate iNOS	[54]
Heart
	In vitro	Myocardial hypertrophy (NMCMs, H9C2 cells)	MA treatment significantly inhibited Ang-II-induced hypertrophy of NMCMs, and the dose did not affect the cell viability of H9C2 and NCMCs	[104]
	In vivo	Myocardial hypertrophy	MA can significantly improve myocardial hypertrophy, myocardial fibrosis and cardiac function, probably through the METTL3-mediated m 6A methylation pathway	[104]
	In vivo	Myocardial hypertrophy	MA reduces stress-overload-induced cardiac hypertrophy in vivo by reducing phosphorylation of AKT and ERK signaling pathways	[105]
	In vivo	Myocardial infarction	MA provides cardioprotection by increasing PON activity, reducing LDL-C levels and inhibiting lipid peroxidation (LPO)	[109]
	In vivo	Myocardial infarction	MA can inhibit the enzyme xanthine oxidase XO to relieve myocardial infarction	[110]
Liver
	In vivo	Acute liver injury	MA inhibits CYP2E1, NF-κB and MAPK pathways, reducing the production of downstream oxidative and inflammatory factors (such as NO, TNF-α and PGE2), ultimately reducing alcohol-induced hepatotoxicity	[126]
	In vivo	Acute liver injury	MA exerts anti-inflammatory and antioxidant effects by inhibiting NF-κB and activating the Nrf2 signaling pathway, thereby providing protection against LPS/D-gal-induced liver injury	[127]
	In vitro	Liver cancer (hepatocellular carcinoma Hep3B, Huh7 and HA22T cells)	MA significantly inhibits angiogenesis and delays the metastasis and invasion of liver cancer cells	[116]
	In vitro	Fatty liver disease	MA can reduce hepatic fat infiltration, restore liver glycogen levels and reduce triglyceride and total cholesterol levels by inhibiting the expression of genes involved in hepatic fat formation	[114]
Stomach
	In vivo	Gastric ulcer	MA pretreatment effectively reduces the area of gastric damage, inhibits H[+] and K[+]-ATPase activity, and provides gastroprotection	[136]
	In vivo	Gastric cancer	MA was able to inhibit IL-6 expression, induce JAK and STAT3 phosphorylation, and down-regulate STAT3-mediated protein Bad, Bcl-2 and Bax expression to treat gastric cancer	[70]
Intestine
	In vitro	Colorectal cancer (HCT116, SW480 cells)	MA mainly induces apoptosis of colorectal cancer cells and inhibits proliferation and migration of colorectal tumors, and induces apoptosis to play an anti-tumor role	[61]
Kidney
	In vivo	Diabetic nephropathy	MA activation of renal AMPK/SIRT1 signaling pathway improves diabetic nephropathy	[42]
	In vivo	Diabetic nephropathy	MA increases renal excretion of Na+ and can also lower blood glucose values	[151]
	In vivo	Renal cell carcinoma	MA inhibited the proliferation of cancer cells by reducing nuclear antigen expression, anti-proliferation and anti-colony production in proliferating cells, and down-regulating VEGF in vascular endothelial cells and PCNA in RCC to inhibit angiogenesis and proliferation	[65]
	In vivo	Acute kidney injury	MA inhibits IRI-induced AKI injury via NF-κB and MAPK signaling pathways	[156]