{"id":63030,"date":"2024-12-30T11:54:07","date_gmt":"2024-12-30T11:54:07","guid":{"rendered":"https:\/\/biomedpharmajournal.org\/?p=63030"},"modified":"2025-01-06T17:53:27","modified_gmt":"2025-01-06T17:53:27","slug":"an-updated-review-of-curcumin-in-health-applications-in-vivo-studies-and-clinical-trials","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol17no4\/an-updated-review-of-curcumin-in-health-applications-in-vivo-studies-and-clinical-trials\/","title":{"rendered":"An Updated Review of Curcumin in Health Applications: In-vivo Studies and Clinical Trials"},"content":{"rendered":"\n

Introduction<\/strong><\/p>\n\n\n\n

Several medicinal\nplants, including rhizomes of turmeric (Curcuma\nlonga<\/em>), ginger (Curcuma xanthorrhiza<\/em>),\nand red ginger (Zingiber officinale<\/em>\nVar. Rubrum), are known to contain curcumin, also referred to as\ndiferuloylmethane (1,7-bis (4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione).\nThis compound is a lipophilic polyphenol belonging to the curcumionide group. Numerous\nin vitro and in vivo studies have demonstrated biological and pharmacological\neffects of curcumin, making it a viable alternative herbal medicine for\ndiseases such as asthma and liver damage. The various functions can be\nattributed to antioxidant, anti-inflammatory, hepatoprotective,\ncardio-protective, antimicrobial, nephroprotective, immunomodulatory,\nhypoglycemic, anti-rheumatic, anti-cancer, and anti-fibrotic properties 1<\/sup>,<\/sup>2<\/sup>.<\/p>\n\n\n\n

Studies on\npharmacological effects of curcumin have produced both positive and negative\nresults. Several tests related to curcumin activity have produced different\neffects 3<\/sup>. The test\ngroup given low-dose curcumin showed positive results in all hepatoprotective\ntest parameters. The amounts of SOD (superoxide dismutase) and MDA\n(malondialdehyde), which helped lower oxidative stress, did not change in the\ntest group given high doses of curcumin. Some researchers report a study on a\npopulation of type 2 diabetes patients, and the results found no change in the\nhs-CRP (high-sensitivity C-reactive protein) test parameters 4<\/sup>. Therefore,\nthis study aimed to explore the therapeutic or placebo effects of curcumin on\nvarious diseases. This review was conducted on the\nlatest literature on clinical trials and animal studies to provide updated\ninformation. Additionally,\nit talks about the outcomes of tests that don’t support the hypothesis or\nsamples that don’t have significant effects.<\/p>\n\n\n\n

Materials and Methods<\/strong><\/strong><\/p>\n\n\n\n

In this\nreview, several journals were collected from PubMed, Scopus, and Science Direct\nwith a maximum limit of the last 8 years. The keywords used include\ncurcuminoid, hepatoprotective, liver, and curcumin health benefits.\nFurthermore, only English-language journals or publications offering open\naccess were used. The inclusion criteria include (a) clinical studies that examined\nthe role of curcuminoid in health benefits; (b) pharmacological activity of\nactive curcuminoid compounds in living organisms; and (c) the possible\npharmacological effects of active curcuminoid on hepatoprotective factors and\nhealth benefits. The\nfindings are then presented in the form of figures and tables, followed by a\nfull discussion based on the appropriate reference. <\/p>\n\n\n\n

Results\nand Discussion<\/strong><\/p>\n\n\n\n

Active Curcuminoid Compounds<\/strong><\/p>\n\n\n\n

Curcumin is a\nnatural yellow hydrophobic polyphenolic pigment that is insoluble in water.\nThis active compound is found in several medicinal plants used in traditional\nmedicines [Figure 1]. Studies have showed pharmacological effects of curcumin,\nmanifesting as antioxidants and anti-inflammatory agents, through mechanisms including\nalterations in gene expression and cellular signaling 5<\/sup>. Turmeric,\nor kencur [Figure 1], is a plant native to India and widely cultivated in areas\nwith temperatures between 20\u25e6<\/sup>C-35\u25e6<\/sup>C and high rainfall, such\nas Indonesia 6,7<\/sup>. <\/p>\n\n\n\n

Rhizomatous\nroots are specifically collected at the end of the vegetative phase when the\nplant can produce therapeutic effects. For decades, several chemical compounds\nfound in ginger have been studied, including oxygenated sesquiterpenes,\nmonoterpenes, and curcuminoid derivative compounds such as curcumin,\nbisdemethoxycurcumin, and demethoxycurcumin 6,8<\/sup>.<\/p>\n\n\n\n\n\n
\"\"<\/td>\n\n

Figure 1: Medicinal plants containing active curcuminoid compounds<\/strong><\/p>\n<\/p>\n

Click here to view Figure<\/a><\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n\n\n

Pharmacological Activity of Curcuminoid Compounds for Health<\/strong><\/p>\n\n\n\n

Studies\non the active compound curcumin have increased in the last few decades due to the\ntherapeutic potential, which spans almost all parts of the human body. Other\nfunctions include antioxidant, anti-inflammatory, human immune regulatory\nsystem, antidiates, nervous system protector, cardiovascular system protector,\nanticancer 9\u201311<\/sup>, arthritis,\nbrain injury, Alzheimer’s, anti-aging, and hepatoprotective effects 12<\/sup>,13<\/sup>,14<\/sup>,15<\/sup>,16<\/sup>. Pharmacological\nactivities reported in the reviewed studies are shown in [Figure 2].<\/p>\n\n\n\n\n\n
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Figure 2: The role of curcuminoid in health for all parts of the human body<\/strong><\/p>\n<\/p>\n

Click here to view Figure<\/a><\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n\n\n

Recent\nclinical and in vivo tests have been carried out to show the emergence of\npharmacological effects of curcumin. Specifically, studies have tested curcumin\nunder predetermined protocols with a wide variety of doses, populations, and\ngroups of animals. Empirical studies assert that plants contain curcumin, a\ncompound with the potential to cure all diseases. This result became the basis\nfor studies developing the effects of curcumin in almost every part of the\nhuman body, with varying degrees of success. Furthermore, numerous in vivo\ninvestigations and clinical trials have been conducted. Tables 1 and 2 show the\nnumerous in vivo studies and clinical trials in sick populations.<\/p>\n\n\n\n

Table 1: In vivo <\/em>studies on active curcuminoid compounds.<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
\n

Active Compounds<\/strong><\/p>\n<\/td>\n

\n

Test Animal Group<\/strong><\/p>\n<\/td>\n

\n

Dose<\/strong><\/p>\n<\/td>\n

\n

Measured parameters<\/strong><\/p>\n<\/td>\n

\n

Reference<\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin<\/p>\n<\/td>\n

\n

32 adult male Wistar rats (200-250 gr)<\/p>\n<\/td>\n

\n

100 mg\/kg\/day for 28 days orally.<\/p>\n<\/td>\n

\n

\u2193ALP, \u2193ASP, \u2193ALT<\/p>\n<\/td>\n

\n

17<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin and the Curcumin Phytosome<\/p>\n<\/td>\n

\n

50 male mice (25-30 g)<\/p>\n<\/td>\n

\n

100-200 mg\/kg body weight orally.<\/p>\n<\/td>\n

\n

Groups III and IV<\/p>\n

\u2191MDA, \u2193SOD, \u2193CAT and \u2193GPx.<\/p>\n

 <\/p>\n

Group V<\/p>\n

\u2193MDA, \u2191SOD, \u2191CAT and \u2191GPx<\/p>\n<\/td>\n

\n

18<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin + dimethylnitrosamine<\/p>\n<\/td>\n

\n

32 Adult male Wistar rats (260~280 g).<\/p>\n<\/td>\n

\n

100 mg\/kg body weight orally.<\/p>\n<\/td>\n

\n

Group III<\/p>\n

\u2193AST, \u2193ALT, and \u2193ALB<\/p>\n

Group IV<\/p>\n

\u2193AST, \u2193ALT, and \u2193ALB<\/p>\n<\/td>\n

\n

19<\/sup><\/p>\n

 <\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin<\/p>\n<\/td>\n

\n

66 Adult male Wistar rats (180-200 g).<\/p>\n<\/td>\n

\n

100-200 mg\/kg body weight orally.<\/p>\n<\/td>\n

\n

Group III<\/p>\n

\u2193ALT, \u2193AST, \u2193AFP, \u2193albumin concentration, \u2193MDA and \u2191SOD<\/p>\n

Group IV<\/p>\n

\u2193ALT, \u2193AST, \u2193AFP, \u2191albumin concentration,<\/p>\n

\u2194 MDA and<\/p>\n

\u2194 SOD, \u2191hepatic lobule physique<\/p>\n<\/td>\n

\n

20<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin + BPA<\/p>\n<\/td>\n

\n

42 Adult male Wistar rats (250\u2013300 g)<\/p>\n<\/td>\n

\n

100-130 mg\/kg body weight orally.<\/p>\n<\/td>\n

\n

Group III<\/p>\n

\u2193MDA, \u2191SOD, \u2191CAT, \u2191GPx and \u2191GST<\/p>\n

Group IV<\/p>\n

\u2193MDA, \u2191SOD, \u2191CAT, \u2191GPx and \u2191GST<\/p>\n

Group V<\/p>\n

\u2191MDA, \u2193SOD, \u2193CAT, \u2193GPx and \u2193GST<\/p>\n

Group VI<\/p>\n

\u2193MDA, \u2191SOD, \u2191CAT, \u2191GPx and \u2191GST<\/p>\n

Group VII<\/p>\n

\u2193MDA, \u2191SOD, \u2191CAT, \u2191GPx and \u2191GST<\/p>\n<\/td>\n

\n

21<\/sup><\/p>\n

 <\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin + Paraquat (PQ)<\/p>\n<\/td>\n

\n

36 Adult male Wistar rats (220\u2013250 g)<\/p>\n<\/td>\n

\n

100 mg\/kg body weight orally.<\/p>\n

 <\/p>\n<\/td>\n

\n

Group V<\/p>\n

\u2193ALT, \u2193AST, \u2193ALP and \u2193MDA<\/p>\n

Group VI<\/p>\n

\u2193ALT, \u2193AST, \u2193ALP and \u2193MDA<\/p>\n<\/td>\n

\n

22<\/sup><\/p>\n

 <\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin<\/p>\n<\/td>\n

\n

24 adult male Wistar rats<\/p>\n<\/td>\n

\n

Curcumin 50 mg\/kg body weight for 12 weeks orally.<\/p>\n<\/td>\n

\n

Group IV (first phase) and Group III (second phase)<\/p>\n

\u2193fibrosis, \u2193liver biomarkers, \u2191CAT, \u2191SOD, \u2191GSH, \u2191electrolyte homeostasis<\/p>\n<\/td>\n

\n

23<\/sup><\/p>\n

 <\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin<\/p>\n<\/td>\n

\n

25 adult male Wistar rats<\/p>\n

(250-280 grams)<\/p>\n<\/td>\n

\n

10-50 mg\/kg body weight, intraperitoneally for 5 weeks.<\/p>\n<\/td>\n

\n

\u2193NLRP3, IL-1\u03b2, IL-6, IL-18, TNF-\u03b1<\/p>\n

\u2191BDNF\/TrkB, PI3K\/Akt signaling pathways<\/p>\n<\/td>\n

\n

24<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin<\/p>\n<\/td>\n

\n

30 adult male Wistar rats (180-200 grams)<\/p>\n<\/td>\n

\n

300 mg\/kg body weight orally for 4 weeks.<\/p>\n<\/td>\n

\n

\u2193Serum creatinine, \u2193urine albumen, and \u2193urea nitrogen enhanced E-cadherin, \u2193LC3 proteins expression, \u2193p62, \u2193phosphorylated levels of Akt, \u2193mTOR, and \u2193P13K levels<\/p>\n<\/td>\n

\n

25<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin<\/p>\n<\/td>\n

\n

30 adult male Wistar rats (200-220 grams)<\/p>\n<\/td>\n

\n

15-60 mg\/kg body weight, through oral gavage.<\/p>\n<\/td>\n

\n

\u2193Inflammation via up-regulating miR-200a-mediated TXNIP and \u2193NLRP3 inflammasome pathway<\/p>\n

 <\/p>\n<\/td>\n

\n

26<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin<\/p>\n<\/td>\n

\n

48 adult male Wistar rats (230-250 grams)<\/p>\n<\/td>\n

\n

200 mg\/kg body weight orally.<\/p>\n<\/td>\n

\n

\u2193Inflammation by downregulation of \u2193TNFa, \u2193IL1b, and \u2193IL 6 Blocked TLR4 \/MyD88\/NFkB<\/p>\n

signal pathways<\/p>\n<\/td>\n

\n

27<\/sup><\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

\u2193significantly decreased, <\/em>\u2191 significantly increased, <\/em>\u2194 showed no effect (still)<\/em><\/p>\n\n\n

Table 2: Clinical Trial <\/em>of active curcuminoid compounds<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
\n

Active Compounds<\/strong><\/p>\n<\/td>\n

\n

Test Animal Group<\/strong><\/p>\n<\/td>\n

\n

Dose<\/strong><\/p>\n<\/td>\n

\n

Measured parameters<\/strong><\/p>\n<\/td>\n

\n

Reference<\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin<\/p>\n<\/td>\n

\n

32 adult male Wistar rats (200-250 gr)<\/p>\n<\/td>\n

\n

100 mg\/kg\/day for 28 days orally.<\/p>\n<\/td>\n

\n

\u2193ALP, \u2193ASP, \u2193ALT<\/p>\n<\/td>\n

\n

17<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin and the Curcumin Phytosome<\/p>\n<\/td>\n

\n

50 male mice (25-30 g)<\/p>\n<\/td>\n

\n

100-200 mg\/kg body weight orally.<\/p>\n

 <\/p>\n

 <\/p>\n<\/td>\n

\n

Groups III and IV<\/p>\n

\u2191MDA, \u2193SOD, \u2193CAT and \u2193GPx.<\/p>\n

Group V<\/p>\n

\u2193MDA, \u2191SOD, \u2191CAT and \u2191GPx<\/p>\n<\/td>\n

\n

18<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin + dimethylnitrosamine<\/p>\n<\/td>\n

\n

32 Adult male Wistar rats (260~280 g).<\/p>\n

 <\/p>\n<\/td>\n

\n

100 mg\/kg body weight orally.<\/p>\n

 <\/p>\n<\/td>\n

\n

Group III<\/p>\n

\u2193AST, \u2193ALT, and \u2193ALB<\/p>\n

Group IV<\/p>\n

\u2193AST, \u2193ALT, and \u2193ALB<\/p>\n<\/td>\n

\n

19<\/sup><\/p>\n

 <\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin<\/p>\n<\/td>\n

\n

66 Adult male Wistar rats (180-200 g).<\/p>\n<\/td>\n

\n

100-200 mg\/kg body weight orally.<\/p>\n

 <\/p>\n<\/td>\n

\n

Group III<\/p>\n

\u2193ALT, \u2193AST, \u2193AFP, \u2193albumin concentration, \u2193MDA and \u2191SOD<\/p>\n

Group IV<\/p>\n

\u2193ALT, \u2193AST, \u2193AFP, \u2191albumin concentration,<\/p>\n

\u2194 MDA and<\/p>\n

\u2194 SOD, \u2191hepatic lobule physique<\/p>\n<\/td>\n

\n

20<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin + BPA<\/p>\n<\/td>\n

\n

42 Adult male Wistar rats (250\u2013300 g)<\/p>\n<\/td>\n

\n

100-130 mg\/kg body weight orally.<\/p>\n<\/td>\n

\n

Group III<\/p>\n

\u2193MDA, \u2191SOD, \u2191CAT, \u2191GPx and \u2191GST<\/p>\n

Group IV<\/p>\n

\u2193MDA, \u2191SOD, \u2191CAT, \u2191GPx and \u2191GST<\/p>\n

Group V<\/p>\n

\u2191MDA, \u2193SOD, \u2193CAT, \u2193GPx and \u2193GST<\/p>\n

Group VI<\/p>\n

\u2193MDA, \u2191SOD, \u2191CAT, \u2191GPx and \u2191GST<\/p>\n

Group VII<\/p>\n

\u2193MDA, \u2191SOD, \u2191CAT, \u2191GPx and \u2191GST<\/p>\n<\/td>\n

\n

21<\/sup><\/p>\n

 <\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin + Paraquat (PQ)<\/p>\n<\/td>\n

\n

36 Adult male Wistar rats (220\u2013250 g)<\/p>\n<\/td>\n

\n

100 mg\/kg body weight orally.<\/p>\n

 <\/p>\n<\/td>\n

\n

Group V<\/p>\n

\u2193ALT, \u2193AST, \u2193ALP and \u2193MDA<\/p>\n

 <\/p>\n

Group VI<\/p>\n

\u2193ALT, \u2193AST, \u2193ALP and \u2193MDA<\/p>\n

 <\/p>\n<\/td>\n

\n

22<\/sup><\/p>\n

 <\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin<\/p>\n<\/td>\n

\n

24 adult male Wistar rats<\/p>\n<\/td>\n

\n

Curcumin 50 mg\/kg body weight for 12 weeks orally.<\/p>\n

 <\/em><\/strong><\/p>\n<\/td>\n

\n

Group IV (first phase) and Group III (second phase)<\/p>\n

 <\/p>\n

\u2193fibrosis, \u2193liver biomarkers, \u2191CAT, \u2191SOD, \u2191GSH, \u2191electrolyte homeostasis<\/p>\n<\/td>\n

\n

23<\/sup><\/p>\n

 <\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin<\/p>\n<\/td>\n

\n

25 adult male Wistar rats<\/p>\n

(250-280 grams)<\/p>\n<\/td>\n

\n

10-50 mg\/kg body weight, intraperitoneally for 5 weeks.<\/p>\n<\/td>\n

\n

\u2193NLRP3, IL-1\u03b2, IL-6, IL-18, TNF-\u03b1<\/p>\n

\u2191BDNF\/TrkB, PI3K\/Akt signaling pathways<\/p>\n<\/td>\n

\n

24<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin<\/p>\n<\/td>\n

\n

30 adult male Wistar rats (180-200 grams)<\/p>\n<\/td>\n

\n

300 mg\/kg body weight orally for 4 weeks.<\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n<\/td>\n

\n

\u2193Serum creatinine, \u2193urine albumen, and \u2193urea nitrogen enhanced E-cadherin, \u2193LC3 proteins expression, \u2193p62, \u2193phosphorylated levels of Akt, \u2193mTOR, and \u2193P13K levels<\/p>\n<\/td>\n

\n

25<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin<\/p>\n<\/td>\n

\n

30 adult male Wistar rats (200-220 grams)<\/p>\n<\/td>\n

\n

15-60 mg\/kg body weight, through oral gavage.<\/p>\n<\/td>\n

\n

\u2193Inflammation via up-regulating miR-200a-mediated TXNIP and \u2193NLRP3 inflammasome pathway<\/p>\n

 <\/p>\n<\/td>\n

\n

26<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Curcumin<\/p>\n<\/td>\n

\n

48 adult male Wistar rats (230-250 grams)<\/p>\n<\/td>\n

\n

200 mg\/kg body weight orally.<\/p>\n<\/td>\n

\n

\u2193Inflammation by downregulation of \u2193TNFa, \u2193IL1b, and \u2193IL 6 Blocked TLR4 \/MyD88\/NFkB<\/p>\n

signal pathways<\/p>\n

 <\/p>\n<\/td>\n

\n

27<\/sup><\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

\u2193significantly decreased, <\/em>\u2191 significantly increased, <\/em>\u2194 showed no effect (still)<\/em><\/p>\n\n\n

Antioxidant Effect<\/strong><\/p>\n\n\n\n

Antioxidant\nactivity of curcumin is one of the several protective mechanisms. Oxidative\nstress is a supporting factor for damage to important organs in the body 42<\/sup>. All cells,\nboth animal and human, require oxygen for normal function to form ATP, which\nthe body then converts into energy through metabolic processes. However,\nreactive oxygen species, which play a role in liver damage, can transfer oxygen\ninto toxic compounds. During the aerobic respiration process, the production of\nfree radicals potentially causes aging and cell death 43<\/sup>.<\/p>\n\n\n\n

Mitochondria\nreduce oxygen molecules to produce superoxide or peroxide ions (H2O2), a free\nradical 44<\/sup>. Superoxide\nand peroxide then react with metal ions and produce hydroxyl radicals.\nSubsequently, hydroxyl radicals react with cell components, including DNA and\nproteins, which can induce damage to the liver 45<\/sup>. The\ntherapeutic potential of polyphenols in curcumin is often associated with\nantioxidant properties, which are able to capture free radicals such as\nsuperoxide or peroxide ions (H2O2). According to a study, curcumin contains 10\ntimes more antioxidants than vitamin E 43<\/sup>.<\/p>\n\n\n\n

The active\ncurcumin compound, with antioxidant effect, effectively binds free radicals and\nprovides hydrogen atoms. Based on chemical structure, the phenolic hydroxyl\ngroup (an electron-donating group) is the main part that makes curcumin an\nantioxidant 11,46<\/sup>. In\nhyperlipidemia disorders, the administration of curcumin can reduce the\nincidence of cardiovascular complications 47,48<\/sup>.<\/p>\n\n\n\n

Anti-inflammatory Agent<\/strong><\/p>\n\n\n\n

During tissue\ndamage from oxidative stress or other factors, inflammation is a response that\nstarts a chain of events leading to repair processes, such as extracellular\nmatrix reform and fibrosis 49<\/sup>. Chronic\ninflammation is defined as macrophage inflammation through tissue invasion and\ncan last for several months to years 50<\/sup>. However,\ncurcumin can turn on PPAR-gamma (Peroxisome Proliferator-Activated\nReceptor-gamma) and stop the production of pro-inflammatory cytokines such as TNF-alpha\nand interleukin-1\u03b2 by blocking signaling pathways including Nf-k\u03b2 (Factor\nNuclear kappa-\u03b2) [Figure 3] 51<\/sup>. The invasion\nprocess of curcumin triggers the expression of inflammatory cytokines or growth\nfactors, closely associated with the pathophysiology of various diseases and\nlifestyles such as cardiovascular disease, obesity, diabetes, myocarditis,\ndementia, atherosclerotic, chronic obstructive pulmonary disease, and other\nconditions 49<\/sup>,52<\/sup>,53<\/sup>. In\ntype 2 diabetes patients, curcumin potentially raises lipid metabolism with a\ndecrease in leptin and an increase in adiponectin levels in the blood 30,54,55<\/sup>. The findings of this\nresearch provide more thorough data on the relationship between curcumin\ndosages and many blood biochemical markers, inflammation, and antioxidants.\nResearch on humans and experimental animals yields almost identical results,\nhowever other investigations showed no significant impacts. In previous\nstudies, there was not much discussion of the parameters that were affected by\nthe use of curcumin.<\/p>\n\n\n\n\n\n
\"\"<\/td>\n\n

Figure 3: Potential mechanism of curcumin in anti-inflammation activity and lifestyle-related conditions (COX2 = cyclooxygenase-2; mPGES-1 = microsomal prostaglandin E synthase-1<\/em>) <\/strong>55<\/sup><\/strong>.<\/strong><\/p>\n

Click here to view Figure<\/a><\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n\n\n

Conclusion<\/strong><\/p>\n\n\n\n

In conclusion,\nvarious studies, both in vivo and clinical, on the test populations in this\nreview showed that curcumin had pharmacological activity in various diseases.\nThe polyphenolic compound had therapeutic potential attributed to the\nantioxidant properties that could capture free radicals. In\nhypercholesterolemia conditions, antioxidant activity reduced enzymes, which had\na major effect on oxidative stress in the liver. Additionally, studies\ndemonstrated anti-inflammatory activity of curcumin, which contributed to the mechanism\nof action in various diseases. The future prospectives of curcumin in health applications can be\ndeveloped in various pharmaceutical preparations, such as nanoparticles, which\nhave the potential to provide higher effects. Comprehensive clinical trials and\nthe potential for drug interactions with other substances molecularly need further\nresearch.<\/p>\n\n\n\n

Acknowledgement<\/strong><\/p>\n\n\n\n

The author would like to thank the\nconsortium team from Universitas Sebelas Maret, Politeknik Elektronika Negeri\nSurabaya, and Politeknik Negeri Madiun for their collaboration in the research\ngrant assignment from the Ministry of Education, Culture, Research, and\nTechnology, Indonesia.<\/p>\n\n\n\n

Funding Sources<\/strong><\/p>\n\n\n\n

This research was funded by Ministry of\nEducation, Culture, Research, and Technology, Indonesia, Directorate General of\nVocational Education with the Applied Research Assignment scheme number:\n37\/SPK\/D.D4\/PPK.01.APTV \/III\/2024 and sub-contract number: 231.1\/UN27.22\/PT.01.03\/2024  with a contract on behalf of Heru Sasongko.<\/p>\n\n\n\n

Conflict of Interest<\/strong><\/p>\n\n\n\n

The author(s) do not\nhave any conflict of interest<\/p>\n\n\n\n

Data Availability Statement<\/strong><\/p>\n\n\n\n

This statement does\nnot apply to this article<\/p>\n\n\n\n

Ethics Statement<\/strong><\/p>\n\n\n\n

This research did\nnot involve human participants, animal subjects, or any material that requires\nethical approval.<\/p>\n\n\n\n

Informed Consent Statement<\/strong><\/p>\n\n\n\n

This study did not\ninvolve human participants, and therefore, informed consent was not required.<\/p>\n\n\n\n

Author Contributions<\/strong><\/p>\n\n\n\n

Heru Sasongko : Conceptualization, Methodology,\nSupervision<\/p>\n\n\n\n

Aulia Hanundita Maharani : Data Collection, Writing \u2013\nOriginal Draft<\/p>\n\n\n\n

Joshua Arianto Hutasoit : Data Collection, Analysis<\/p>\n\n\n\n

Darmawan Lahru Riatma : Editing <\/p>\n\n\n\n

Hardian Ningsih : Project Administration<\/p>\n\n\n\n

Sritrusta Sukaridhoto : Supervision<\/p>\n\n\n\n

Mohammad Robihul Mufid : Editing<\/p>\n\n\n\n

MH. Ramdhani Ismar : Project Administration<\/p>\n\n\n\n

Ardian Prima Atmaja : Editing<\/p>\n\n\n\n

Alfi Tranggono Agus Salim: Visualization<\/p>\n\n\n\n

Ronny Martien : Supervision<\/p>\n\n\n\n

References<\/strong><\/p>\n\n\n\n

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