International Journal of Medical Sciences And Clinical Research
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VOLUME
Vol.05 Issue04 2025
PAGE NO.
24-30
10.37547/ijmscr/Volume05Issue04-05
Basic Treatment of Peptic Ulcer Disease in Folk Medicine
with Plantago And Hypericum Linariifolium
Ibragim Askarov
Andijan State University, Andijan, Uzbekistan
Khabibullo Kodirov
Andijan Medical Institute, Andijan, Uzbekistan
Received:
24 February 2025;
Accepted:
20 March 2025;
Published:
23 April 2025
Abstract:
Data on rejuvenation and a rise in individuals with ulcerative colitis, one of the most prevalent
gastroenterological conditions worldwide, are examined in this study. The research of the causes of this illness
and the impact of the medications now used to treat it on the human div receive the majority of focus. The
chemical makeup of medicinal plants used to treat it, the biological activity of the food additive " Plantago and
Hypericum linariifolium " the suggested methods of use and mechanisms of action for the disease's prevention
and treatment, and the pertinent conclusions were all examined.
Keywords:
Peptic ulcer disease, plantago, hypericum linariifolium, chromatogram, polyphenols.
Introduction:
People who have peptic ulcer disease
develop abnormalities (ulcers) in their stomach and/or
duodenum. The majority of peptic ulcer disease
patients are men between the ages of 20 and 50, and
their numbers are steadily rising each. The illness is
cyclical and has a chronic course, deteriorating the
host's health over years as periods of aggravation are
interspersed with false quiet. In spring and fall, the
ulcer typically manifests.It is interesting to note that
duodenal ulcers are far more common than stomach
ulcers.
An open sore that appears on the stomach's inner lining
or the duodenum, the upper portion of the small
intestine, is called a peptic ulcer. It happens when the
protective membrane of these organs is harmed by
stomach
acid.Peptic
Ulcer
Disease
(PUD)
epidemiology.Globally, peptic ulcer disease (PUD),
which encompasses duodenal and stomach ulcers, is a
prevalent gastrointestinal ailment. Geographical
location, age, gender, and risk factors including NSAID
usage and H. pylori infection all affect its prevalence.
Worldwide Prevalence: Five to ten percent of people
are thought to have PUD overall. NSAID-related ulcers
are more prevalent in industrialized countries, whereas
H. pylori-related ulcers are more prevalent in
underdeveloped countries.
Many nations have shown declining trends in the
incidence of PUD as a result of greater use of proton
pump inhibitors (PPIs), decreased H. pylori infection,
and improved cleanliness. Distribution by Age and
Gender: More prevalent in older persons, particularly
those over 50, as a result of decreased mucosal
protection and greater NSAID usage. While stomach
ulcers are more common in elderly persons (over 60),
duodenal ulcers are more common in younger adults
(30
–
50 years old). The male-to-female ratio for
duodenal ulcers is 2:1, meaning that males are more
afflicted than women.Disparities by Region: Developing
nations: higher prevalence (up to 80
–
90% of ulcers) as
a result of H. pylori infection. Developed nations:
NSAID-related ulcers are on the rise, although H. pylori
incidence are lower. Asia:
Greater prevalence of stomach ulcers, particularly in
East Asia (China, Korea, Japan), may be brought on by
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International Journal of Medical Sciences And Clinical Research (ISSN: 2771-2265)
genetic and nutritional factors. Western nations: More
NSAID-related ulcers due to higher aspirin and NSAID
usage.Risk factors that influence the epidemiology of
PUD:
1Infection with H. pylori is the cause of 50
–
70% of
ulcers
in
affluent
nations
and
80
–
90%
in
underdeveloped nations.
2. NSAID usage is responsible for 30
–
40% of ulcers,
particularly in older adults.
3. Drinking drink and smoking raises the risk of ulcers
and slows their repair.
4. Stress: linked to elevated acid production,
particularly in patients in severe condition.
5. Dietary factors: Caffeine and spicy foods can
exacerbate symptoms but are not the cause.
Peptic Ulcer Disease Pathogenesis (PUD)When the
stomach and duodenal mucosa's defensive (protecting)
and aggressive (destructive) components are out of
balance, Peptic Ulcer Disease (PUD) results. NSAID
usage, increased stomach acid production, and H.
pylori infection are the main reasons.
Aggressive and defensive factors are out of balance.
Factors that are aggressive (damaging): an infection
with H. pylori. Pepsin and gastric acid (HCl). NSAIDs,
such as Naproxen, Ibuprofen, and Aspirin. reflux of bile.
Stress, alcohol, and smoking. The mucus-bicarbonate
barrier, which neutralizes acid and shields the
epithelium, is one defensive (protective) factor. Blood
flow is maintained and mucus and bicarbonate
production is stimulated by prostaglandins (PGE2,
PGI2). mechanisms for the renewal and repair of
epithelial cells. sufficient blood flow over the mucosa.
causes of ulcer development. Ulcers Caused by A. H.
pylori (Most Common Cause).
Chronic inflammation is brought on by H. pylori
colonizing the stomach mucosa, particularly the
antrum.. The urease enzyme neutralizes stomach acid
and promotes bacterial viability by converting urea into
ammonia. CagA and VacA are cytotoxins: harm
epithelial cells, exacerbate inflammation, and hinder
the healing process. TNF-
α, IL
-1, IL-6, and other forms
of inflammation: promotes acid secretion and impairs
mucosal defenses. Mucous layer disruption: Causes
direct injury from pepsin and acid, which results in ulcer
formation.
Duodenal ulcers: H. pylori raises gastrin levels, which
causes excessive acid production and damage to the
duodenal mucosa.Gastric ulcers: H. pylori reduces the
production of protective mucus by causing mucosal
inflammation and atrophy. B. Ulcers Caused by NSAIDs.
By: Blocking cyclooxygenase (COX-1 and COX-2)
enzymes → ↓ prostaglandin synthesis → ↓ mucus and
bicarbonate production, NSAIDs (Aspirin, Ibuprofen,
and Naproxen) harm the stomach lining.
Loss of prostaglandin inhibition results in an increase in
the release of stomach acid. decreasing blood supply to
the mucosa, which causes ischemia and slows healing.
The stomach, not the duodenum, is where the majority
of NSAID-induced ulcers develop.C. Gastric acid
hypersecretion (Zollinger-Ellison syndrome). Excessive
acid production from pancreatic or duodenal
gastrinomas, or tumors that secrete gastrin, results in
severe ulcers.Peptic Ulcer Complications Untreated
ulcers may result in: Bleeding in the stomach (caused
by blood vessel erosion). Perforation: an ulcer that
erodes through the wall of the stomach or duodenum.
occlusion of the gastric outflow (caused by edema and
scarring).
The location, etiology, clinical course, and endoscopic
appearance of peptic ulcers can all be used to
categorize them. according to the location.The
stomach's smaller curvature is often where gastric
ulcers occur.More frequent than stomach ulcers,
duodenal ulcers develop in the first section of the
duodenum. according to the etiology (cause)
Helicobacter pylori infection is the cause of H. pylori-
associated ulcers.ulcers brought on by long-term use of
NSAIDs (such as ibuprofen and aspirin). Stress ulcers,
such as Cushing's ulcer in brain damage and Curling's
ulcer in burn patients, form in critically sick patients as
a result of extreme stress, trauma, burns, or
infection.Ulcers associated with Zollinger-Ellison
syndrome (ZES) are brought on by an overabundance
of acid produced by tumors that secrete gastrin
(gastrinomas). Idiopathic ulcers, which have no known
origin, are frequently observed in younger people.
Аccording to the clinical course. Acute ulcers appear
rapidly and are frequently brought on by
extreme stress, trauma, or NSAID usage.Chronic ulcers
are persistent, frequently brought on by an H. pylori
infection or prolonged use of NSAIDs, and they
frequently flare up.
Jensen's classification for bleeding ulcers is based on
endoscopic appearance. used to determine the peptic
ulcer bleeding risk:Spurting arterial bleeding (type Ia)
carries the highest risk of rebleeding. Type Ib: Seeping
hemorrhage. Type IIa: Non-bleeding vessel that is
visible. Adherent blood clot, type IIb. Type IIc: A
pigmented patch that is flat. Clean-based ulcers (type
III) have the lowest chance of bleeding again.according
to pathological characteristics. Benign ulcers are
spherical, smooth, and have uniform edges. The
uneven, elevated borders of malignant ulcers are
frequently linked to stomach cancer. Peptic Ulcer
Disease (PUD) symptoms. There are some distinctions
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International Journal of Medical Sciences And Clinical Research (ISSN: 2771-2265)
between the symptoms of duodenal and stomach
ulcers, but they might be identical.
Common signs and symptoms. Upper abdominal
discomfort that burns or gnaws (epigastric pain).
usually takes place at night or in between meals.may
come and go and last anywhere from minutes to hours.
feeling full and bloated right after eating. vomiting and
nausea. Acid reflux disease, or heartburn. weight loss
and appetite loss. The distinctions between duodenal
and stomach ulcers. Severe symptoms (complications):
you need to see a doctor right away. Hematemesis, or
blood in the vomit, might seem red or like coffee
grounds. Melena, or tarry, black stools, is caused by
digested blood. Sharp, severe stomach discomfort
might be a sign of a perforation. Abrupt weakness,
lightheadedness, or fainting might be signs of anemia
or hemorrhage peptic ulcer
Imaging scans, laboratory testing, and clinical
evaluation are all used in the diagnosis of duodenal and
stomach ulcers. Clinical Assessment, Symptoms, and
History: NSAID usage, H. pylori risk factors, and
epigastric discomfort in connection to meals. Physical
examination: May show serious consequences (stiff
abdomen in perforation), anemic symptoms (pallor), or
minor epigastric discomfort. Tests in the Lab Testing for
H. pylori (to ascertain cause). The most accurate non-
invasive test is the urea breath test. stool antigen test,
which is commonly utilized. Blood-based serologic
testing (which finds antibodies but not actual
infections). Rapid urease test combined with
endoscopic biopsy (gold standard if endoscopy is
done).To check for anemia (low hemoglobin) brought
on by bleeding, perform a complete blood count (CBC).
The Fecal Occult Blood Test (FOBT) finds blood in the
stool that is concealed and indicates a bleeding ulcer.
Imaging and Endoscopic Research. The gold standard
for identifying peptic ulcers is upper gastrointestinal
(GI)
endoscopy,
often
known
as
esophagogastroduodenoscopy, or EGD.
enables direct visibility, therapy (such as cauterizing
bleeding ulcers), and biopsy (to rule out stomach
cancer). X-ray of barium meals (Upper GI Series). used
in the absence of endoscopy.
Although less precise than endoscopy, it can identify
ulcers,
perforations,
or
obstructions.Extra
examinations for severe or resistant ulcers. Gastrin
Levels (Fasting Serum Gastrin Test) in the event that
excessive acid production, or Zollinger-Ellison
Syndrome (ZES), is suspected. biopsies to screen for
stomach cancer. carried out during an endoscopy for
suspected or non-healing stomach ulcers.To increase
precision and early diagnosis, non-invasive testing,
high-resolution imaging, and molecular techniques are
the mainstays of contemporary diagnostic approaches
for gastric and duodenal ulcers.
By improving mucosal and vascular features,
advanced endoscopic techniques such as High-
Resolution Endoscopy (HRE) with Narrow Band Imaging
(NBI) make it easier to distinguish between benign and
malignant ulcers. Particularly for stomach ulcers,
endoscopic ultrasound (EUS) aids in determining the
depth of the ulcer and identifying cancer. To evaluate
H. pylori infection and malignant alterations, confocal
laser
endomicroscopy
(CLE)
offers
real-time
microscopic imaging of ulcer tissue. AI-Based Diagnosis
for Endoscopic Procedures Artificial intelligence (AI)
systems examine endoscopic pictures to identify ulcers,
distinguish them from malignancy, and forecast the
likelihood of bleeding. Non-invasive detection of
Helicobacter pylori. Labeled Urea Breath Test (UBT): ¹³C
or ¹⁴C. A non
-invasive, very reliable test for identifying
an active H. pylori infection. Mass spectrometry is used
in contemporary breath tests to improve accuracy.
PCR-Based Stool Antigen Test (SAT) & ELISA-Based
possesses good sensitivity for detecting H. pylori
antigens. Even after exposure to antibiotics, PCR-based
assays enhance detection. Tests for urine and saliva
(Emerging Methods). Although less popular, it is being
developed for simpler, at-home testing. Biomarker and
molecular testing. Next-Generation Sequencing (NGS)
and PCR for H. pylori
finds the DNA of H. pylori in saliva, feces, or stomach
biopsies. finds the genes that cause antibiotic
resistance,
allowing
for
more
individualized
therapy.Serum Pepsinogen Test (Marker for Gastric
Atrophy) .
Low levels of pepsinogen The I/II ratio indicates a risk
of stomach ulcers or chronic gastritis. Gastrin-17 Test.
assesses gastrin levels, which is helpful in the diagnosis
of atrophic gastritis and Zollinger-Ellison syndrome
(ZES).Innovations in Imaging Multiphoton Microscopy
(MPM) offers cellular-level real-time imaging of
stomach
tissue.
Contrast-enhanced
magnetic
resonance imaging (MRI) aids in the detection of
abnormalities and problems of the stomach wall, such
as cancer or perforation.
CT angiography. used to identify the bleeding
vessel prior to endoscopic treatment in situations of
significant ulcer bleeding. Endoscopy using Smart
Capsules (PillCamTM) a wireless camera in a capsule
that takes pictures while it passes through the digestive
system. helpful in identifying minor duodenal ulcers
when conventional endoscopy yields conflicting
results.Targeting the H. pylori infection, lowering
stomach acid production, shielding the mucosa, and
avoiding complications are the main goals of the
International Journal of Medical Sciences And Clinical Research
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International Journal of Medical Sciences And Clinical Research (ISSN: 2771-2265)
contemporary treatment of gastric and duodenal
ulcers. Based on patient-specific variables, ulcer
severity, and antibiotic resistance, the treatment is
becoming more and more individualized.
H. pylori eradication (if present) The primary cause of
peptic ulcers is an H. pylori infection, which must be
eradicated in order to promote healing and stop
recurrence. Triple therapy, or first-line therapy.
Omeprazole, Esomeprazole, or Pantoprazole are
examples of proton pump inhibitors (PPIs).
Clarithromycin and Amoxicillin (or Metronidazole in the
case of a penicillin allergy) are two antibiotics. Time
frame: 10
–
14 days.If clarithromycin resistance is
detected, second-line therapy (also known as
quadruple therapy) is used. Metronidazole +
Tetracycline + Bismuth Subsalicylate + PPI. Time frame:
10
–
14 days.
Customized Treatment (Predicated on Antibiotic
Resistance) H. pylori resistance genes are found using
molecular assays (PCR, NGS). In situations of resistance,
levofloxacin-based treatment is employed.
Therapy for acid suppression. Prolonged acid
suppression encourages ulcer healing and keeps them
from coming back.First Choice: Proton Pump Inhibitors
(PPIs). Dexlansoprazole, Rabeprazole, Esomeprazole,
Pantoprazole, or Omeprazole. superior to H2 blockers
in effectiveness. 4
–
8 weeks are needed for full
recovery. A more recent substitute is potassium-
competitive acid blockers, or P-CABs. Compared to
PPIs, vonoprazan is a stronger and quicker-acting acid
suppressor.Very good in eliminating H. pylori and ulcers
caused by NSAIDs.
For mild cases, H2-Receptor Blockers (H2RAs) are an
alternative. Famotidine and ranitidine are less often
used since PPIs work better.
Protective agents for mucosa. These medications
support healing and strengthen mucosal protection.
Sucralfate: Covers the ulcer with a protective layer. A
component of quadruple treatment, bismuth
subsalicylate also possesses antibacterial properties
against Helicobacter pylori. Misoprostol, an analog of
prostaglandin, reduces ulcers caused by NSAIDs (not
recommended during pregnancy). Treatment of Ulcers
Caused by NSAIDs. If at all feasible, stop using NSAIDs.
Use PPIs or Misoprostol for protection if NSAIDs are
necessary (for example, in individuals with arthritis).
Safer alternatives are COX-2 inhibitors, such as
celecoxib and etoricoxib.
Surgical
and
endoscopic
procedures
(for
complications). Treatments with endoscopy (for
bleeding ulcers). Endoscopic Hemostasis (injection
treatment, hemoclips, or electrocoagulation).
A contemporary powder spray for halting severe
bleeding
is
Endoscopic
Spray
with
HemosprayTM.surgery that is minimally invasive. For
perforated ulcers, laparoscopic ulcer repair is used. For
recurring ulcers that are not improving with
medication, vagotomy may be necessary.
Emerging and Regenerative Therapies. Research on the
regeneration of the stomach mucosa by stem cell
therapy. Epidermal growth factors (EGF) are used in
growth factor therapy to promote mucosal repair.
Probiotics are part of microbiome-based therapy,
which promotes gut healing following H. pylori
treatment.
Traditional Treatments for Peptic Ulcer For ages, peptic
ulcers have been treated with traditional and folk
treatments with Plantago and Hypericum linariifolium,
which frequently aim to lower inflammation, shield the
stomach lining, and encourage healing. Although these
treatments can alleviate symptoms, they should be
used in conjunction with traditional medication as
supportive therapy rather than as a substitute for
medical care.
Changes in Diet and Lifestyle Steer clear of greasy,
acidic, and spicy foods that upset the stomach.Cut back
on alcohol and coffee.In order to avoid acid
accumulation, eat smaller, more frequent meals. Use
breathing techniques, yoga, or meditation to reduce
stress.
Summary of the Modern Approach: 1. Eradication of H.
pylori (specific antibiotic treatment). 2. PPI treatment
(or Vonoprazan in cases of resistance). 3. Mucosal
defense (Misoprostol, Bismuth, and Sucralfate).
Prevention of NSAID ulcers (PPI + COX-2 inhibitors).5.
Surgical and endoscopic treatment of problems.
METHOD
Determination of the amount of phenolic compounds
in the extract in the YUSSCH method Used jet and
equipment. Gallic acid h
as been isolated from” Macklin
“(China), salicylic acid from” Rhydburg Pharmaceuticals
“(Germany), quercetin, apigenin, kempferols from”
Regal " (China), rutin from natural sources in extraction
and column chromatography techniques. Water,
acetonitrile, chemically pure brand acetic acid and
sodium hydroxide reagents were used at HPLC level
purity.
The column thermostat was set at 40 oC, the injection
volume was set at 10 MCL, and the flow rate was set at
0.5 ml/min. At 300 Nm, the phenolic compound
analytical signal (peak area) was captured (Figure 1).
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International Journal of Medical Sciences And Clinical Research (ISSN: 2771-2265)
Table 1.
Phase gradient program.
Time
Atsetonitril (A), %
0.5% acetic acid (B), %
0
5
95
5
5
95
17
40
60
22
40
60
22,1
5
95
40
Finish
Figure 1. Chromatogram of standards at 300 nm.
RESULTS
Determination of the amount of phenolic compounds
in the sample extract. A chromatogram of a sample
extract with a mass of 1 g was taken (Figure 2), and
based on the results, the amounts of phenol
compounds in a sample of 100 g were calculated with
the formula below and brought in Tables 3.
𝑋 =
𝐶
𝑝ℎ𝑒𝑛
∙ 𝑉
𝑒𝑘𝑠𝑡𝑟𝑎𝑐𝑡
𝑚
𝑆𝐴𝑀𝑃𝐿𝐸
∙ 100 𝑔
Here, the amount of phenolic compounds in x-100
grams of fruit, mg;
C phen is the concentration of an extract containing
phenol compound determined by the Yussch method,
mg / l;
V ekstrakt-sample extract size, l;
M sample the mass of a sample weighed to make an
extract.
Figure 2. Chromatogram for the determination of polyphenols in the sample extract.
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International Journal of Medical Sciences And Clinical Research (ISSN: 2771-2265)
Table 2. The amount of polyphenols in the extract and the capture Times.
Phenol compound
name
Capture
time,
SEC
Concentration,
mg / l
100 g sample
quantity, mg
Gallic acid
0
0
0,000
Rutin
18,403
4,867
12,168
Salicylic acid
22,208
7,352
18,380
Quercetine
24,564
2,695
6,738
Apigenin
27,778
8,987
22,468
Kaempferol
28,282
18,096
45,240
The amount of polyphenols contained in the plant was
carried
out
in
the
high-performance
liquid
chromatograph LC-40 Nexera Lite, made at Shimadzu in
Japan.
standard solutions' preparation. In an ultrasonic bath,
5.2 mg of gallic acid, 5.2 mg of salicylic acid, 5 mg of
rutin, 5 mg of quercetin, 5 mg of apigenin, and 5 mg of
kempferol were dissolved in 96% ethanol for 20
minutes. The mixture was then transferred to a 50 ml
flask and sent to the line with ethanol. Using 200 µL of
each solution, four distinct solutions were made, which
were then combined by peeling. The Viala was filled
with each solution and utilized for analysis.
In order to extract phenolic chemicals, 1 g of the
material under examination was drawn with an
accuracy of 0.01 g using the OHAUS Company's (USA)
nv222 brand Scale. It was then put in a 50 ml conical
flask and 25 ml of 96% ethanol was added. The mixture
was extracted for 20 minutes at 60 oC in an ultrasonic
bath bearing the GT SONIC-D3 (Chinese) trademark.
After cooling and filtering, the liquid was transferred to
a measuring flask containing 25 milliliters of ethanol. In
a mini-7 brand (BIOBASE, China) centrifuge, 1.5 ml of
the extract (7000 ayl) was centrifuged at a high speed,
filtered through a 0.45 µm screw filter, and then
utilized for analysis.
identification of phenolic substances. A gradient motile
phase (Table 1) comprising a 0.5% li solution (B) of
acetonitrile (A) and acetic acid in water was used,
together with a standard solution and a sample extract
Shim pack GIST C18 (150 × 4.6 mm; 5 µm, Shimadzu,
Japan) reverse phase colon.
CONCLUSION
Traditional Treatments for Peptic Ulcer For ages, peptic
ulcers have been treated with traditional and folk
treatments, which We discovered how crucial it is to
treat patients by giving them a biologically active
supplement to take in addition to their primary
medications. Using shun, we were able to determine
the phenolic qualities of these therapeutic herbs and
found that our indicators are high and will help us in the
future when we develop yanda for patients.
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