As we all know "flux" which originated in pine rosin is incredibly useful, pretty much essential in soldering. This is because it acts as an antioxidant neutralizing coating of oxidized metal which prevents metals from binding. Well, Ive been kind of curious about the various properties of rosin for a while.
I recently found this paper.
"In this paper, we describe several bioactive terpenoids
(Figure 2) contained in herbal or dietary plants, which
have the potential to ameliorate metabolic disorders via
activation of ligand-dependent transcription factors, namely,
peroxisome proliferator-activated receptors (PPARs)."
This is an important use because of the epidemic of obesity which may have environmental causes.
Its possible that the main constituent in flux may be valuable in fighting the metabolic syndrome which is characterized by systemic inflammation.
"Recently, it has been indicated that obesity is associated
with a low-grade chronic inflammation state [34]. The
inflammatory condition in obesity is increasingly being
recognized as an important contributor to the development
of metabolic syndrome and its associated complications.
Adipocytes can secret cytokines involved in inflammation,
such as adiponectin, monocyte chemoattractant protein-1
(MCP-1), and tumor necrosis factor-α (TNF-α) [35]. MCP-
1, a member of the CC chemokine superfamily, plays a piv-
otal role in monocyte/macrophage trafficking and activation
[36]. Macrophages also produce various proinflammatory
factors including MCP-1 and TNF-α. Macrophage-derived
TNF-α establishes a vicious cycle that augments inflamma-
tory changes and insulin resistance in obese adipose tissues
[37]. Therefore, to prevent obesity-related inflammation, it
is important to decrease the production of obese-adipose-
tissue-derived proinflammatory factors such as MCP-1 and
TNF-α.
Several herbal and dietary plants improve medical con-
ditions including diabetes mellitus, hyperlipidemia, and car-
diovascular disease associated with an abnormality of lipid
metabolism [38, 39]. To screen for novel natural ligands for
PPARs, we have evaluated PPAR ligand activities for various
terpenoids in an advanced highly sensitive system with
the coexpression of a coactivator for nuclear receptors, the
cAMP-response element-binding protein (CREB)-binding
protein (CBP), developed by modifying the luciferase
reporter assay system [40]. Hereinafter, we describe several
terpenoids, identified as novel PPAR ligands, in our PPAR
ligand screening."
........
Here they describe the compounds we are familiar with...
".3. Abietic Acid Derivatives. The amount of variety of
hydrocarbons and their derivatives used in industrial and
commercial activities has been increasing over the years.
Abietic acid is a tricyclic-diterpene carboxylic acid (Figure 2),
and is the main component of the rosin fraction of oleoresin
synthesized by conifer species, such as grand fir (Abies gran-
dis) and lodgepole pine (Pinus contorta) [58]. Abietic acid is
commonly used as a fluxing agent in solder, as a paper sizing
agent to make paper more water resistant, and in printing
inks, adhesives, and plasticizers [59]. Moreover, it has been
reported that abietic acid is a bioactive compound and it has
an anti-inflammatory effect. In lipopolysaccharide (LPS)-
stimulated macrophages, abietic acid suppresses production
of prostaglandin E2 (PGE2) in vitro and in vivo [60].
To investigate whether the activation of PPARs is related
to the anti-inflammatory effects of abietic acid and its
derivatives, we evaluated the effects of abietic acid and its
derivatives on PPAR activity (Figure 2). Abietic acid and
dehydroabietic acid, one of major components of colophony
(also known as Rosin and pine resin), potently activated
both PPARα and PPARγ but not PPARδ [61, 62]. Similarly
to thiazolidinedione, a synthetic PPARγ ligand, abietic acid
suppressed mRNA expressions of TNF-α and cyclooxygenase
2 (COX2), which are induced in inflammatory reactions,
in LPS-stimulated macrophages [61]. Dehydroabietic acid
stimulated PPARα and PPARγ more potently than abietic
acid [62]. Dehydroabietic acid significantly suppressed the
production of proinflammatory mediators such as MCP-
1, TNF-α, and NO in LPS-stimulated macrophages and in
the coculture of macrophages and adipocytes [62]. In obese
diabetic KK-Ay mice, dietary dehydroabietic acid suppressed
obesity-associated elevation of circular MCP-1 and TNF-α
levels and their mRNA expressions in white adipose tissues.
Moreover, dehydroabietic acid improved carbohydrate and
lipid metabolism [63]. These findings indicate that the
anti-inflammatory effects of abietic acid and dehydroabietic
acid are at least partly due to the activation of PPARs.
Additionally, it is suggested that these compounds can be
used not only for anti-inflammation but also for regulating
carbohydrate and lipid metabolism and atherosclerosis."
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So, anyway, our understanding of the mechanisms underlying adiposity are changing, and inflammation is at the core of our new knowledge. We may be able to address obesity somewhat by restoring people to a less inflammatory state with compounds that modulate the activity of the PPARs.
http://downloads.hindawi.com/journals/ppar/2010/483958.pdf