High‐density lipoprotein: A potent inhibitor of inflammation

1. Inflammation is an important process, driving the progression of atherosclerosis. Stemming inflammation may be a mechanism to inhibit the progression of this disease. 2. High‐density lipoprotein (HDL), a particle inversely related to cardiovascular disease, has been described as having a number of anti‐inflammatory functions. It has been shown that HDL inhibits endothelial inflammation in both in vitro and in vivo models, reducing the expression of key cell adhesion molecules. In addition, HDL has been shown to have an effect on the coagulation pathway by inhibiting platelet activation and reducing thrombus formation. Furthermore, by reducing the activation of leucocytes, HDL can inhibit leucocyte recruitment to the endothelium. 3. High‐density lipoprotein infusion studies conducted in patients with inflammatory diseases have shown that acute treatment with HDL can effectively inhibit inflammation in vivo. Thus, HDL has been proven to be a potent inhibitor of inflammation, acting on a number of pathways, and this may suggest that HDL could be applied as an anti‐inflammatory molecule for a number of diseases. 4. The present review highlights these important studies and reviews data on the anti‐inflammatory effects of HDL from in vitro and in vivo studies, in both humans and animal models of atherosclerosis and inflammatory‐related diseases.     

Is Minocycline an Antiviral Agent? A Review of Current Literature

Minocycline is a second‐generation semi‐synthetic derivative of tetracycline and has well‐known anti‐bacterial effects. The drug possesses anti‐inflammatory, anti‐oxidant, anti‐apoptotic and immunomodulatory effects. The drug is widely used in bacterial infections and non‐infectious conditions such as acne, dermatitis, periodontitis and neurodegenerative conditions. Minocycline was shown to have antiviral activity in vitro and also against different viruses in some animal models. Some studies have been done on human patients infected with Human Immunodeficiency Virus. We have review the available data regarding minocycline activity as an antiviral agent.     

Simvastatin and Indomethacin Have Similar Anti‐Inflammatory Activity in a Rat Model of Acute Local Inflammation

Abstract: Statins, such as simvastatin, lower circulating cholesterol levels and are widely prescribed for the treatment of hypercholesterolaemia. Several studies have shown unexpected effects of statins on inflammation. We studied the anti‐inflammatory effect of simvastatin using a standard model of an acute local inflammation, the carrageenan‐induced footpad oedema. Experimental groups (n = 6–8) were given simvastatin in a dose range 5–30 mg/kg, indomethacin 1–8 mg/kg and methylcellulose (control) per os. Footpad volume was measured with a plethysmograph and compared with the pre‐injection volume of the same paw. Swelling (in microlitres) was then calculated, and in drug‐treated animals, per cent inhibition was derived through comparison with the control group. Histopathological examination of the skin biopsies was performed to examine severity of paw skin lesions and to confirm the simvastatin‐induced inhibition of acute inflammation. Both simvastatin and indomethacin administered orally, 1 hr before carrageenan injection, significantly reduced the extent of footpad oedema. Indomethacin dose‐dependently blocked the swelling; the maximal effect was obtained with 8 mg/kg by 48.3% (P < 0.05). Simvastatin produced a comparable anti‐inflammatory activity at a dose of 5 mg/kg (32%), while 10 and 30 mg/kg caused a 47.6% and 51.7% reduction, respectively, with the maximal effect observed at 20 mg/kg by 57.2% (P < 0.05). The comparison of the ED₅₀ of these agents on molar basis showed equipotent anti‐inflammatory activity. Histopathological examination of the footpad skin biopsies revealed that simvastatin, dose‐dependently and comparablly to indomethacin, reduced polymorphonuclear leucocyte infiltration. These data support the hypothesis that simvastatin has an acute anti‐inflammatory activity.     

Synthesis and evaluation of anti‐inflammatory properties of silver nanoparticle suspensions in experimental colitis in mice

The aim of our study was to investigate the effect of newly developed silver nanoparticle aqueous suspensions NanoAg1 and NanoAg2 in the mouse models mimicking ulcerative colitis and Crohn's disease. NanoAg1 and NanoAg2 were synthesized in aqueous medium with the involvement of tannic acid. To elucidate their anti‐inflammatory activity, semi‐chronic mouse models of inflammation induced by dextrane sulfate sodium addition to drinking water and intracolonic (i.c.) administration of 2,4,6‐trinitrobenzenesulfonic acid were used. NanoAg1 and NanoAg2 (500 mg/dm3, 100 μl/animal, i.c., once daily) significantly ameliorated colitis in dextrane sulfate sodium‐ and 2,4,6‐trinitrobenzenesulfonic acid‐induced mouse models of colonic inflammation, as indicated by reduced macroscopic, ulcer and microscopic scores. The anti‐inflammatory effect was dependent on the shape and diameter of silver nanoparticles, as indicated by weaker effect of NanoAg1 than NanoAg2. In addition, administration of NanoAg2, but not NanoAg1, modulated colonic microbiota, as indicated by reduced number of Escherichia coli and Clostridium perfringens, and increased number of Lactobacillus sp. Summarizing, NanoAg1 and NanoAg2 after administered i.c. effectively alleviate colitis in experimental models of ulcerative colitis and Crohn's disease in mice. Therefore, NanoAg1 and NanoAg2 administered i.c. have the potential to become valuable agents for the treatment of inflammatory bowel diseases.     

Anti-inflammatory activity of the non-peptidyl low molecular weight radical scavenger IAC in carrageenan-induced oedema in rats

Objective In this research we investigated the anti‐inflammatory activity of a non‐peptidyl low molecular weight radical scavenger (IAC) in an acute and chronic animal model of inflammation. Methods For this purpose the effect of IAC (10, 25, 50 mg/kg) was tested in rats on the associated behavioral responses to subsequent inflammatory and noxious challenges, such as hind paw oedema induced by intra‐plantar injection of carrageenan and granuloma induced by subcutaneous implant of a cotton pellet, using indometacin (2.5 mg/kg) as reference drug. Moreover, the serum level of several cytokines was tested in the animal treated (or not) with IAC (50 mg/kg) both in the absence and presence of carrageenan‐induced inflammation. Key findings IAC showed a significant anti‐inflammatory activity in both in acute and chronic models of inflammation. In addition IAC down regulated significantly the serum levels of interleukin (IL) 2 and IL6 whereas it increased the serum concentration of IL1α and glutathione. Conclusion Although it remains to be elucidated whether or not the antioxidant property of IAC is directly responsible for the modulation of the tested cytokines, these results suggest IAC to be a possible candidate for a novel anti‐inflammatory compound     

Discovery of naphthyl‐N‐acylhydrazone p38α MAPK inhibitors with in vivo anti‐inflammatory and anti‐TNF‐α activity

Protein kinases constitute attractive therapeutic targets for development of new prototypes to treat different chronic diseases. Several available drugs, like tinibs, are tyrosine kinase inhibitors; meanwhile, inhibitors of serine/threonine kinases, such as mitogen‐activated protein kinase (MAPK), are still trying to overcome some problems in one of the steps of clinical development to become drugs. So, here we reported the synthesis, the in vitro kinase inhibitory profile, docking studies, and the evaluation of anti‐inflammatory profile of new naphthyl‐N‐acylhydrazone derivatives using animal models. Although all tested compounds ( 3a–d ) have been characterized as p38α MAPK inhibitors and have showed in vivo anti‐inflammatory action, LASSBio‐1824 ( 3b ) presented the best performance as p38α MAPK inhibitor, with IC₅₀ = 4.45 μm , and also demonstrated to be the most promising anti‐inflammatory prototype, with good in vivo anti‐TNF‐α profile after oral administration.     

Anti‐inflammatory Effect of Rosmarinic Acid and an Extract of Rosmarinus officinalis in Rat Models of Local and Systemic Inflammation

Rosmarinic acid is a polyphenolic compound and main constituent of Rosmarinus officinalis and has been shown to possess antioxidant and anti‐inflammatory properties. We aimed to evaluate the anti‐inflammatory properties of rosmarinic acid and of an extract of R. officinalis in local inflammation (carrageenin‐induced paw oedema model in the rat), and further evaluate the protective effect of rosmarinic acid in rat models of systemic inflammation: liver ischaemia–reperfusion (I/R) and thermal injury models. In the local inflammation model, rosmarinic acid was administered at 10, 25 and 50 mg/kg (p.o.), and the extract was administered at 10 and 25 mg/kg (equivalent doses to rosmarinic acid groups) to male Wistar rats. Administration of rosmarinic acid and extract at the dose of 25 mg/kg reduced paw oedema at 6 hr by over 60%, exhibiting a dose–response effect, suggesting that rosmarinic was the main contributor to the anti‐inflammatory effect. In the liver I/R model, rosmarinic acid was administered at 25 mg/kg (i.v.) 30 min. prior to the induction of ischaemia and led to the significant reduction in the serum concentration of transaminases (AST and ALT) and LDH. In the thermal injury model, rosmarinic acid was administered at 25 mg/kg (i.v.) 5 min. prior to the induction of injury and significantly reduced multi‐organ dysfunction markers (liver, kidney, lung) by modulating NF‐κB and metalloproteinase‐9. For the first time, the anti‐inflammatory potential of rosmarinic acid has been identified, as it causes a substantial reduction in inflammation, and we speculate that it might be useful in the pharmacological modulation of injuries associated to inflammation.     

Hypoxia inducible factor‐1α inhibition produced anti‐allodynia effect and suppressed inflammatory cytokine production in early stage of mouse complex regional pain syndrome model

Complex regional pain syndrome (CRPS) is related to microcirculation impairment associated with tissue hypoxia and peripheral cytokine overproduction in the affected limb. Previous studies suggest that the pathogenesis involves hypoxia inducible factor‐1α (HIF‐1α) and exaggerated regional inflammatory response. 1‐methylpropyl 2‐imidazolyl disulfide (PX‐12) acts as the thioredoxin‐1 (Trx‐1) inhibitor and decreases the level of HIF‐1α, and can rapidly be metabolized for Trx‐1 redox inactivation. This study hypothesized that PX‐12 can decrease the cytokine production for nociceptive sensitization in the hypoxia‐induced pain model. CD1 mice weighing around 30 g were used. The animal CRPS model was developed via the chronic post‐ischaemic pain (CPIP) model. The model was induced by using O‐rings on the ankles of the mice hind limbs to produce 3‐h ischaemia–reperfusion injury on the paw. PX‐12 (25 mg/kg, 5 mg/kg) was given through tail vein injection immediately after ischaemia. Animal behaviour was tested using the von Frey method for 7 days. Local paw skin tissue was harvest from three groups (control, 5 mg/kg, 25 mg/kg) 2 h after injection of PX‐12. The protein expression of interleukin‐1β (IL‐1β) and HIF‐1α was analysed with the Western blotting method. Mice significantly present an anti‐allodynia effect in a dose‐related manner after the PX‐12 administration. Furthermore, PX‐12 not only decreased the expression of HIF‐1α but also decreased the expression of IL‐1β over the injured palm. This study, therefore, shows the first evidence of the anti‐allodynia effect of PX‐12 in a CPIP animal model for pain behaviour. The study concluded that inhibition of HIF‐1α may produce an analgesic effect and the associated suppression of inflammatory cytokine IL‐1β in a CPIP model.     

Solidagenone from Solidago chilensis Meyen inhibits skin inflammation in experimental models

Solidagenone (SOL) is a labdane‐type diterpenoid found in Solidago chilensis, a plant traditionally used to treat skin diseases, kidney pain and ovarian inflammation. In this study, the topical anti‐inflammatory activity of SOL was evaluated using in vivo and in silico assays. Croton oil‐, arachidonic acid (AA)‐ and phenol‐induced ear oedema mouse models were applied in the in vivo studies. Myeloperoxidase (MPO) and N‐acetyl‐β‐D‐glucosaminidase (NAG) activities and tumour necrosis factor alpha (TNF‐α), interleukin‐6 (IL‐6) and nitric oxide (NO) levels were determined, as well as histopathological analyses were conducted. Interaction profiles between SOL and cyclooxygenase‐1 (COX‐1), cyclooxygenase‐2 (COX‐2), glucocorticoid receptor, estradiol‐17‐β‐dehydrogenase and prostaglandin‐E(2)‐9‐reductase were established using molecular docking. SOL significantly inhibited croton oil‐, AA‐ and phenol‐induced ear oedema (P < .001) at doses of 0.1, 0.5 and 1.0 mg/ear. The MPO and NAG activities and TNF‐α, IL‐6 and NO levels were decreased (P < .001). The histopathological data revealed that inflammatory parameters (oedema thickness, leucocyte infiltration and vasodilatation) were reduced by treatment with SOL at doses of 0.1, 0.5 and 1.0 mg/ear. The docking study showed that SOL interacts with COX‐1 and prostaglandin‐E(2)‐9‐reductase through hydrogen bonding, inhibiting these enzymes. These results indicate that SOL may be a promising compound for the treatment of cutaneous inflammatory disorders and has potential as a topical anti‐inflammatory agent.     

Adipose‐derived mesenchymal stem cells therapy for acute kidney injury induced by ischemia‐reperfusion in a rat model

Acute kidney injury (AKI) represents a group of complicated syndromes with a high mortality rate. The administration of adipose‐derived mesenchymal stem cells (ADMSCs) has been tested as a possible treatment method for AKI. The long‐term evaluation of AKI induced by ischemia/reperfusion (IR) and the probable renal protection of ADMSCs are limited. In this study we have established a rat AKI model induced by IR and investigated the possible protective effects of ADMSCs. Adult Sprague‐Dawley (SD) rats were divided into three groups (n = 6/each group). The MOCK group was as the normal control. Rats in the IR‐AKI and IR‐AKI+ADMSCs groups were subjected to IR injury by clamping both renal pedicles for 40 minutes. Rats in the MOCK and IR‐AKI groups were injected with PBS via the tail vein as negative treatment controls. Rats in the IR‐AKI+ADMSCs group received ADMSCs therapy (2 × 10⁶ cells were injected into the rats via the tail vein). We found that ADMSC transplantation restored the pathologic morphology induced by IR‐AKI to normal compared with the MOCK group, suggesting the reparative function of ADMSCs in kidney tissues. Compared with IR‐induced AKI alone, ADMSC treatment significantly decreased the number of apoptotic cells, the level of total urinary protein and serum creatinine, the expression of pro‐inflammatory cytokines (IL‐6, TNF‐α, IL‐1β, IFN‐γ, TNF‐α, IFN‐γ, and TGF‐β), and the inflammation‐associated proteins (HGF and SDF1), but increased the expression of the anti‐inflammatory cytokine, IL‐10, and the anti‐apoptotic regulator, Bcl‐2. Our data have indicated that ADMSC transplantation may protect against IR‐induced AKI by anti‐apoptotic and anti‐inflammatory effects.     

Curcumin alleviates lung injury in diabetic rats by inhibiting nuclear factor‐κB pathway

Curcumin is a polyphenolic compound that is extracted from Curcuma longa. It has broad anti‐inflammation and anti‐tumor activities. Curcumin was previously reported to exert beneficial effects on diabetes. However, the effect of curcumin on diabetes‐induced lung injury is not yet clear. In this study, the effects of curcumin on lung injury induced by diabetes was explored using quantitative real time polymerase chain reaction (PCR), enzyme‐linked immunosorbent assay (ELISA), immunohistochemistry and electrophoretic mobility shift assay. The results of this study showed that curcumin reduced oxidative stress level, inhibited the synthesis of nitric oxide and prostaglandin E2, and reduced inflammatory responses in the lungs of diabetic rats, thereby alleviating diabetes‐induced lung injury. Further study of the mechanism revealed that curcumin inhibited the activation of nuclear factor (NF)‐κB which is a key player in inflammatory responses. In summary, our study demonstrated that curcumin inhibited the activation of NF‐κB in the lungs of diabetic rats, thus reducing pulmonary inflammatory responses and oxidative stress, and ultimately relieving diabetes‐induced lung injury. This study suggests that curcumin may be a promising agent to alleviate diabetic lung injury and also provides theoretical foundation for the development of diabetes therapy.     

Zinc against advanced glycation end products

Advanced glycation end products (AGEs) are destructive compounds with pathogenic importance in age‐related chronic diseases. Zinc has antioxidant, anti‐inflammatory and anti‐apoptotic potential. This study aimed to summarize effects of zinc on AGE formation and AGE‐induced damaging agents. Pubmed, Google scholar, Web of Sciences, and Scopus databases were searched. There was no limitation for publication date. English language original articles (in vitro, experimental and human studies) which examined the effect of external zinc on AGE formation, AGE‐induced apoptosis, or oxidative stress in mammals were included. To review the effect of zinc on AGE generation, the search keywords were as follows: “zinc” in title and “AGEs” or “methylglyoxal” or “pentosidine” or “carboxymethyllysine” or “glucosylation” or “carbonyl stress” or “AGEs‐induced apoptosis or oxidative stress or inflammation” in title/abstract. In total, 90 titles and abstracts were identified. Fifty‐two studies were screened after duplicates were removed. Six articles were chosen for review following analysis of both titles and summaries. Finally, based on intensive critical appraisal, 5 articles were included in the study. The evidence presented indicates that zinc has anti‐glycation, anti‐oxidative and anti‐apoptotic effects. Zinc insufficiency may stimulate AGEs formation. Whereas, zinc supplementation could inhibit formation of AGEs, AGE‐induced cell apoptosis and oxidative stress status, and protein carbonyl formation possibly through various signalling pathways.     

Anti‐inflammatory properties of resveratrol in the retinas of type 2 diabetic rats

Resveratrol (trans‐3,5,4′‐trihydroxystilbene) is a nutritional supplement with anti‐inflammatory properties. The present study investigated the long‐term anti‐inflammatory property of resveratrol in the retinas of type 2 diabetic rats. Male Wistar rats were divided into four groups: normal control, diabetic control, resveratrol‐treated normal rats and resveratrol‐treated diabetic rats. Type 2 diabetes was induced by a single dose injection of streptozotocin (50 mg/kg; i.p.) 15 min after the administration of nicotinamide (110 mg/kg; i.p.) in 12‐h fasted rats (the streptozotocin–nicotinamide type 2 diabetic model). Oral resveratrol administration (5 mg/kg per day for 4 months) significantly improved glucose tolerance, and alleviated hyperglycemia and weight loss in diabetic rats. Furthermore, resveratrol administration significantly decreased the elevated levels of nuclear factor‐κB activity, and mRNA expression, tumour necrosis factor alpha level and apoptotic cells in the retinas of the diabetic rats. Furthermore, resveratrol did not significantly affect plasma insulin levels. Long‐term resveratrol administration has beneficial anti‐inflammatory properties in a rat model of diabetes. However, whether resveratrol exerts its effects directly or through reducing blood glucose levels requires further investigation.     

Tropisetron ameliorates early diabetic nephropathy in streptozotocin‐induced diabetic rats

It has been well established that oxidative stress and inflammation are involved in the pathogenesis of diabetic nephropathy. It has been shown that tropisetron exerts anti‐inflammatory and immunomodulatory properties. The current study was designed to investigate protective effects of tropisetron on early diabetic nephropathy in streptozotocin‐induced diabetic rats. Rats were divided into six groups: (i) untreated diabetic (streptozotocin group); (ii) untreated control; (iii) diabetic rats treated with tropisetron (3 mg/kg); (iv) normal rats treated with tropisetron (3 mg/kg); (v) diabetic rats treated with granisetron (3 mg/kg); and (vi) normal rats treated with granisetron (3 mg/kg); rats began receiving treatment at the time of diabetes induction for 2 weeks. At the termination of the experiments, bodyweight, kidney index, urinary albumin excretion, and glomerular filtration rate were measured. The levels of oxidative stress markers and tumour necrosis factor‐α were also determined. Streptozotocin‐treated animals showed significant loss of bodyweight and renal enlargement and dysfunction. Diabetic rats also exhibited an increase in malondialdehyde along with a significant decrease in glutathione, superoxide dismutase activity, and catalase activity. Furthermore, the diabetic animals demonstrated a significant rise in renal cortical, urinary tumour necrosis factor‐α, and urinary albumin excretion. Both granisetron and tropisetron decreased blood glucose in diabetic animals, but this decrease was not significant for granisetron. Treatment with tropisetron, but not granisetron, prevented increases in oxidative stress and tumour necrosis factor‐α, decreased urinary cytokine excretion and albuminuria, and improved renal morphological damage. In conclusion, the present study suggests that tropisetron may be a protective agent in early diabetic nephropathy, and its action is mediated, at least in part, by anti‐oxidative and anti‐inflammatory mechanisms that appear to be independent of the 5‐HT₃ receptor.     

Effects of pioglitazone and vildagliptin on coagulation cascade in diabetes mellitus – targeting thrombogenesis

Introduction: Type 2 diabetes mellitus (T2DM) is intricately allied with an increased risk of atherothrombotic disease. Thrombosis is the cause of mortality in 80% of patients with diabetes mellitus. Endothelial abnormalities lead to elevated inflammatory and coagulation biomarkers as seen in diabetes. Progression of atherothrombotic disease in diabetes has been linked with elevated levels of various coagulation factors including fibrinogen, plasminogen activator inhibitor-1, and von Willebrand factor.

Areas covered: We review the existing evidence and most recent data elucidating the various inflammatory and coagulation biomarkers that are elevated in T2DM leading to thrombosis as well as the anti-inflammatory, anticoagulant and antithrombotic mechanisms of pioglitazone and vildagliptin in addition to their effect on glucose metabolism that may halt the progression of atherothrombotic disease.

Expert opinion: The review highlights the pleiotropic effects of pioglitazone and vildagliptin on metabolic, inflammatory and coagulation processes that have the potential to influence cardiovascular disease progression at various points in the disease process, including hemostatic disturbances, inflammation, plaque rupture and atherogenesis in T2DM. Finally, the paper suggests a possible decline in T2DM-associated cardiovascular comorbidities once the antithrombotic potential of pioglitazone and vildagliptin is established through clinical investigation.     

Structure–Activity Relationship of Terpenes with Anti‐Inflammatory Profile – A Systematic Review

Inflammation is a complex biological response that in spite of having available treatments, their side effects limit their usefulness. Because of this, natural products have been the subject of incessant studies, among which the class of terpenes stands out. They have been the source of study for the development of anti‐inflammatory drugs, once their chemical diversity is well suited to provide skeleton for future anti‐inflammatory drugs. This systematic review reports the studies present in the literature that evaluate the anti‐inflammatory activity of terpenes suffering any change in their structures, assessing whether these changes also brought changes in their effects. The search terms anti‐inflammatory agents, terpenes, and structure–activity relationship were used to retrieve English language articles in SCOPUS, PUBMED and EMBASE published between January 2002 and August 2013. Twenty‐seven papers were found concerning the structural modification of terpenes with the evaluation of anti‐inflammatory activity. The data reviewed here suggest that modified terpenes are an interesting tool for the development of new anti‐inflammatory drugs.     

Ameliorative effects of riboflavin on acetic acid‐induced colonic injury in rats

Riboflavin (RF) has been found to be a promising antioxidant and/or anti‐inflammatory agent in several studies. However, the effect of RF against acetic acid (AA)‐induced colonic injury is currently unknown. This study aimed to investigate the potential antioxidant and protective effects of RF in a rat model of ulcerative colitis. Starting immediately after the colitis induction (AA+RF group) or 1 week before the colitis induction (RF+AA+RF group), the rats were treated with RF (25 mg/kg per day; p.o.) for 3 days. The control and AA groups received saline (1 mL; p.o.) whereas AA+SS group (positive control) received sulfasalazine (100 mg/kg per day; p.o.) for 3 days. Colonic samples were taken for the biochemical and histological assessments on the third day. High damage scores, elevated tissue wet weight index (WI), tissue myeloperoxidase (MPO) activity, 8‐hydroxy‐2′‐deoxyguanosine levels and chemiluminescence values, and a pronounced decrease in antioxidant glutathione (GSH) levels of the AA group were all reversed by RF pretreatment (RF+AA+RF group) and SS treatment (AA+SS group) (P < .05‐.001). Tissue WI, MPO activity and GSH levels were not statistically changed in the AA+RF group. Western blot analysis revealed that the decreased protein expressions of tissue collagen (COL) 1A1, COL3A1 and transforming growth factor‐β1 in the AA group were elevated in all the treatment groups (P < .05‐.001). In conclusion, RF exerts both the antioxidant and anti‐inflammatory effects against AA‐induced colonic inflammation by suppressing neutrophil accumulation, inhibiting reactive oxidant generation, preserving endogenous glutathione, improving oxidative DNA damage and regulating inflammatory mediators, suggesting a future potential role in the treatment and prevention of ulcerative colitis.     

Review article: anti‐fibrotic agents for the treatment of Crohn’s disease – lessons learnt from other diseases

Background The current therapies for Crohn’s disease (CD) are mainly focused on blockade of inflammation. Fibrosis remains one of the major complications of CD often leading to surgery, affecting patients’ quality‐of‐life. Aim To summarize the published data regarding the potential anti‐fibrotic role of drugs commonly used in CD and the most effective anti‐fibrotic drugs used in other diseases evaluating their potential use to treat intestinal fibrosis in CD. Methods A literature search was performed in the PubMed, Medline, Cochrane and EMBASE databases, considering in vitro, animal and human studies on fibrosis in inflammatory bowel disease and other similar chronic pathologies. Results Treatment of fibrosis in CD is limited to surgery or endoscopic dilatation, although some of the drugs currently used may have anti‐fibrotic activity. In other diseases, anti‐fibrotic agents are already used or are in preclinical or clinical trials. ACE inhibitors, Angiotensin Receptor Blockers, and HMG‐CoA inhibitors merit further investigation in CD because of their role in preventing fibrosis in cardiovascular and renal diseases. Conclusions Anti‐fibrotic drugs are under evaluation or already used in clinical practice in other chronic inflammatory diseases. In CD, there is a great need for investigation into agents that may prevent, reduce or reverse intestinal fibrosis. Aliment Pharmacol Ther 31 , 189–201